
<*-££. 










Class rNV . 3A \ 
Book , Y f ffi 
GpightN 

CQFVRIGIIT DEPOSIT. 




PLATE I 



Opaque Optic-Nerve Fibres. — (After Beard.) — This is aeon- 
genital condition of the fundus oculi, in which the medullary 
substance of the optic-nerve fibres continues out over the 
retina instead of stopping at the papilla as it normally 
should do. In this condition and location we obtain the most 
direct and complete observation of the intact nervous tissue 
during life that it is possible to have. 



A TREATISE 

ON 



DISEASES 



OF THE 



NERVOUS SYSTEM 

BY 

L. HARRISON METTLER, A.M., M.D. 

Associate Professor of Neurology, College of Medicine of the 
University of Illinois; Professor of Mental and Nervous 
Diseases in the Chicago Clinical School; Con- 
sulting Neurologist to the Norwegian 
Deaconess' Home and Hospital, 
Chicago. 



Complete in One Volume 



grofusetu ^Illustrated 



CLEVELAND PRESS 
CHICAGO 

1905 



LIBRARY Of CONGRESS 
Two Copies Received' 

DEC 22 1904 

^Copyrutm entry 

CUSS JO XXc, Noj 

copy b. 



Copyright 1904 

BY THE 

CLEVELAND PRESS 

CHICAGO 



PREFACE 



The Neurone Doctrine is now an accepted fact. Its teachings 
have done more to illuminate the dark places of neurology than has any 
single scientific generalization heretofore promulgated. In spite of the 
fact that in regard to many of its details much has yet to be learned, 
the main principles which it lays down are universally acknowledged 
to be scientifically accurate and practically useful. The present treatise 
has been written with the view of presenting the subject of neurology 
in consonance with this doctrine. The diseases are classified, so far as 
possible, upon that basis. The neuronic structure of the nervous sys- 
tem is given special emphasis. And the role of the neurone in the 
matter of the pathology and symptomatology of these diseases is kept 

well in view. The author feels that the time has arrived for the frank 

* 
recognition of this great doctrine, not merely in histology but also in 

the greater field of neurology. He is convinced that one cannot acquire 
a proper conception of modern neurology without an adequate knowl- 
edge of the neuronic structure of the nervous system. Mistakes in the 
diagnosis and blunders in the treatment of diseases of the nervous sys- 
tem can be minimized only by keeping well in mind the facts taught in 
the neurone theory. If the present volume will enable the student and 
the practitioner to behold the entire field of neurology — modern neu- 
rology — under the brilliant illumination cast upon it by this scientific 
generalization, the highest wish of the author will have been attained. 
The unity of the nervous apparatus and its functions, the author 
believes, is not to-day taught as emphatically as it should be. In 
some quarters the tendency is marked to discuss the nervous system 
and its diseases in such minute detail that the universal working of the 
nervous system as a single, uniform, albeit compound organ, seems to 
have been lost sight of. This is shown particularly in connection with 
the subject of the cerebral localizations. Psychology is a science as 
well as neurology ; and as neurosis underlies psychosis, it is incumbent 
that a proper conception of modern psychology should be possessed to 
fully comprehend the nature of the cerebral localizations, the psychic 
symptoms of nearly all the nervous affections and the entire psychic 
side of neurology. The author has endeavored to make plain from the 



O PREFACE 

standpoint of modern psychology many of the psycho-physical manifes- 
tations of the nervous organ. 

In the presentation of the individual diseases, their diagnosis and 
pathology have been especially dwelt upon, the writer being of the 
firm opinion that treatment and general therapeutics are absolutely 
valueless — sometimes positively dangerous — in the absence of a cor- 
rect or approximately correct diagnosis. Neurology's hardest prob- 
lems are in the diagnostic sphere. Given a correct diagnosis, the treat- 
ment is generally a very simple affair. Diagnosis and pathology rest 
upon anatomy and physiology, hence much space has been given to 
normal as well as abnormal neurology in the following work. 

The proper classification of some nervous affections is still a mat- 
ter of uncertainty. One has but to recall such troubles as the myo- 
pathies, the periodical paralyses, Landry's paralysis, certain types of 
polyneuritis, exophthalmic goitre, progressive facial hemiatrophy, my- 
asthenia gravis. Bell's mania, disseminated sclerosis, hypertrophic 
pachymeningitis and many others. The author has classified them in 
accordance with his own view and with what he believes to be the 
general view among the best authorities. 

For valuable assistance and helpful suggestions the author feels 
his indebtedness to many friends and desires to avail himself of this 
opportunity to thank especially Dr. Walter M. Fitch for some exquisite 
photographic work ; Dr. Charles H. Beard, Dr. Oscar Dodd and Dr. 
Willis O. Nance for their ophthalmological assistance ; Dr. G. B. 
Hassin and others. 

Grateful acknowledgment is also extended to the various publish- 
ing firms who have courteously permitted the use of illustrations from 
works issued by them. 

L. H. M. 



TABLE OF CONTENTS 



SECTION A. 



INTRODUCTION. 

Peculiarities of the Nervous System and its diseases ly 

Classification of nervous diseases 22 

Etiology of the diseases of the nervous system 25 

Degeneracy 29 

Pathology of the diseases of the nervous system 35 

Symptomatology and Diagnosis of the diseases of the nervous sys- 
tem 41 

Examination of the patient 42 

Electro-diagnosis 64 

Treatment of the diseases of the nervous system 75 



SECTION B. 



THE NEURONIC DISEASES. 

The Neurone and the Neuronic structure of the nervous system . . 89 

The Neurone Doctrine 89 

The Neuronic Architecture of the nervous system 96 

The Neuroses 101 

a. The cerebrospinal neuroses 102 

Hysteria 102 

Psychoneuroses related to Sleep and Hysteria 138 

Dreams 141 

Pavor nocturnus 141 

Nightmare 141 

Automatism 142 

Somnambulism 142 

Hypnotism and hypnosis 143 

Catalepsy 146 



TABLE OF CONTEXTS 

Lethargy 146 

Insomnia 146 

Prolonged sleep 148 

Sleeping sickness. Negro lethargy 148 

Vertigo 149 

Ocular vertigo 152 

Aural vertigo. Meniere's disease 153 

Neurasthenia 157 

Hypochondriasis 173 

The Traumatic Neuroses 182 

Epilepsy 188 

Myoclonus-epilepsy 207 

I Icmicrania. Migraine 221 

I Ieadache. Cephalalgia 234 

The Neuralgias 242 

Tic douloureux, prosopalgia 248 

Glossodynia . . . , 250 

Occipital neuralgia 250 

Cervico-brachial neuralgia 251 

Mastodynia 251 

Lumbar neuralgia 251 

Coccydynia 251 

Pododynia 252 

Visceral neuralgia 252 

Spermatic neuralgia . 252 

Urethrodynia 252 

Eclampsia 252 

Eclampsia infantum . . 25 2 

Eclampsia parturientium 254 

Eclampsia unemica 255 

Te tany. Tetanilla 2^6 

I .ocalized myospasms 262 

1 a icalized Spasmodic Tic. Tic convulsif 264 

I ; aeial tic 

A I asticatory tic 266 

I [ypoglossal tic 266 

Tic of the trunk and extremities 266 

Respiratory tic 266 

Spasmodic torticollis 267 

Spasmus nutans 268 

I reneral Tic. Tic impulsif 269 

"Jumpers," Mirvaelnt, Latah 270 



TABLE OF CONTEXTS 9 

Paramyoclonus multiplex 271 

Occupation Neuroses 272 

Myotonia congenita 284 

The Choreas 286 

Acute Minor chorea. Sydenham's chorea 287 

Symptomatic chorea 297 

Chronic hereditary (Huntington's) chorea 297 

Electric chorea 299 

Paralysis agitans. Shaking palsy 299 

b. The sympathetic neuroses. Angioneuroses and trophoneu- 
roses 306 

The Sympathetic Nerve ; anatomy and physiology 306 

Symmetrical gangrene. Raynaud's disease 310 

Erythromelalgia 314 

Acroparsesthesia 316 

Angioneurotic oedema ' 318 

Chronic hereditary trophcedema '. 321 

Intermittent articular hydrops 321 

Exophthalmic goitre 322 

Athyrea 334 

Myxcedema 335 

Cretinism 337 

Acromegaly 339 

Gigantism 343 

Adiposis dolorosa 345 

Scleroderma 346 

Progressive facial hemiatrophy 348 

Ainhum 350 

The System Diseases 350 

Their nature and classification 350 

Diseases of the Afferent or Sensory System 367 

Locomotor ataxia 367 

Diseases of the Efferent or Motor System 392 

Progressive muscular atrophy 392 

Amyotrophic lateral sclerosis 401 

Progressive bulbar paralysis 406 

Progressive muscular dystrophy 409 

Pseudo-hypertrophic paralysis 416 

Juvenile dystrophy 418 

Infantile dystrophy 418 

Spastic paraplegia of adults 421 

Spastic paraplegia of childhood 425 



10 TABLE OF CONTENTS 

Secondary spastic paralyses 426 

Ophthalmoplegia 427 

Myasthenia gravis 429 

Occupation muscular atrophy. Craft palsy 430 

Acute ascending (Landry's) paralysis 431 

Periodical paralysis 436 

Diseases of the Afferent and Efferent Systems 437 

Ataxic paraplegia 439 

Hereditary ataxia 444 

Friedreich's disease 444 

Amaurotic family idiocy 451 

Multiple neuritis and neuromyelitis 454 

Progressive interstitial hypertrophic neuritis 454 



SECTION C 



THE NON-NEURONIC DISEASES. 

The Nature of the non-neuronic diseases 457 

Part I. Non-neuronic diseases of the Spinal Cord 459 

The Spinal Cord ; its anatomy and physiology 459 

Spinal localization and topography 485 

Lumbar puncture 494 

Diseases of the Spinal Column 496 

Dislocations and fractures of the vertebrse 496 

Caries of the vertebrse. Tubercular spondylitis 499 

Tumors of the vertebrse 507 

Syphilitic disease of the vertebrse 509 

Aneurismal erosion of the vertebrse 509 

Spinal hydatid disease 509 

Lateral curvature of the spine 509 

Arthritis deformans of the spine 510 

Diseases of the Membranes of the Spinal Cord 511 

Ansemia and hypersemia 511 

Inflammation of the spinal membranes. Meningitis 512 

External pachymeningitis 512 

Chronic cervical hypertrophic pachymeningitis 514 

Acute spinal leptomeningitis 516 

Syphilitic spinal meningitis. Spinal syphilis 519 

Spinal meningeal hemorrhage. Hematorrhachis 524 



TABLE OF CONTENTS II 

Diseases of the Spinal Cord 526 

Anaemia 527 

Hyperemia 527 

Embolism. Thrombosis. Endarteritis 528 

Spinal hemorrhage. Hematomyelia 528 

Myelitis 531 

Acute anterior poliomyelitis of infants 541 

Poliomyelitis of adults , . . . 552 

Abscess of the cord 555 

Tumors of the spinal cord 555 

Cavities of the spinal cord 562 

Hydromyelia 563 

Syringomyelia 563 

Malformations of the cord. Spina bifida 569 

Caisson disease 570 

Diseases of the Cauda Equina and Filum Terminate 573 

Part II. N on-neuronic diseases of the Peripheral Nerves 576 

The Peripheral Nerves ; their anatomy and physiology 576 

Neuritis 581 

Multiple neuritis 589 

Alcoholic multiple neuritis 592 

Lead multiple neuritis 595 

Arsenical multiple neuritis 597 

Argentic multiple neuritis 598 

Mercurial multiple neuritis 598 

Diphtheritic multiple neuritis 599 

Rheumatic multiple neuritis 602 

Puerperal multiple neuritis 602 

Beriberi or Kakke 603 

Akatama 603 

Leprous multiple neuritis 604 

Tumors of the Nerves. Neuromata 600 

Multiple neuromata 609 

Fibroma molluscum multiplex 6og 

Plexiform neuroma 610 

Diseases of the Spinal Nerves 613 

Phrenic nerve 613 

The brachial plexus 614 

Erb's palsy 616 

Klumpke's palsy 616 

Total plexus palsy 616 

Obstetrical palsy 617 



12 TABLE OF CONTENTS 

Posterior or long thoracic nerve 617 

Circumflex nerve 618 

Musculo-cutaneous nerve 61 8. 

Suprascapular nerve 618 

Musculo-spiral nerve 619 

Median nerve 621 

Ulnar nerve . 622 

The dorsal nerves 624 

The lumbar plexus 624 

Obdurator nerve 626 

Anterior crural nerve 626 

The sacral plexus 626 

Sciatic nerve. Sciatica 627 

Plantar nerves » 635 

The muscles of the body, their functions and nerve supply 636 

Diseases of the Cranial Nerves 643 

Oculomotor or third nerve 646 

Trochlear or fourth nerve 648 

Abducens or sixth nerve 64S 

Trifacial or fifth nerve 649 

Facial or seventh nerve 652 

Auditory or eighth nerve 657 

( ilossopharyngeal or ninth nerve 658 

Pneumogastric or tenth nerve 659 

Accessorius or eleventh nerve 660 

1 Iypoglossal or twelfth nerve 661 

I 'art III. Xon-neuronic diseases of the Brain 662 

The Brain, its anatomy 662 

Weight of the brain 664 

Membranes of the brain 1 

Embryological development 668 

Lobes, convolutions, fissures, sulci 672 

Cranio-cerebral topography 677 

Minute structure of the brain 680 

Cortex 68l 

( Ufactory lobes (>S<> 

Corpora striata 6 

( )ptic thalami 691 

( )ptic tracts and retina . . . .692 

Regio subthalamic^ 695 

Corpora quadrigemina (105 

Peduncles «»i" the brain 1 



TABLE OF CONTENTS I 



Cranial nerve nuclei -. 698 

Olivary bodies 705 

Cerebellum -...■, . . . 705 

Cerebellar cortex 707 

Conducting tracts of the brain 710 

Circulation of the brain . 710 

Brain physiology and cerebral localization 714 

Cortex ...;.. 717 

Internal capsule . 736 

Corpus callosum ......: 736 

Corpora striata 737 

Optic thalami 737 

Corpora quadrigemina, geniculate bodies and pulvinar 73S 

Red nucleus, etc 739 

Corpora mamillaria 739 

Hypophysis cerebri ............. 739 

Epiphysis cerebri ,.-..■ 739 

Crura cerebri 739 

Pons and medulla . . ..»....: 740 

Cerebellum .....:...;...... 740 

Olivary bodies 741 

Symptoms of diseases of the brain . . -749 

General symptoms . . 751 

Psychic symptoms - 753 

Disturbances of language . 763 

Motor symptoms 772 

Sensory symptoms .....:.... yyy 

Olfactory symptoms 779 

Optic symptoms 780 

Gustatory symptoms 792 

Auditory symptoms , . . . 792 

Diseases of the Membranes of the Brain 793 

Pachymeningitis 793 

Hsematoma 794 

Leptomeningitis 798 

Acute leptomeningitis .798 

Epidemic cerebrospinal meningitis ........... 808 

Tuberculous meningitis 814 

Chronic meningitis 820 

Circulatory diseases of the Brain 821 

Cerebral anaemia 822 

Cerebral hyperemia 825 



14 TABLE OF CONTENTS 

Cerebral hemorrhage 828 

Encephalomalacia. Embolism and thrombosis 845 

Thrombosis of the intracranial veins and sinuses 850 

Infantile hemiplegia 854. 

Encephalitis 864 

Acute hemorrhagic encephalitis 865 

Acute suppurative encephalitis ; cerebral abscess 867 

Acute delirium. Bell's mania 874 

Cerebral syphilis 877 

Dementia paralytica. General paresis 888 

Multiple sclerosis 901 

Tumor of the brain 909 

Intracranial aneurism 934 

Hydrocephalus 937 

Serous meningitis 939 

Acquired chronic hydrocephalus 941 

Congenital hydrocephalus . . 942 

Diseases of the Pons Varolii and Medulla oblongata. 

Acute superior polioencephalitis 951 

Acute inferior polioencephalitis 952 

Apoplectiform bulbar paralysis 952 

Diseases of the Cerebellum 954 

Malformations of the Brain 956 



SECTION D. 



GENERAL MALADIES WITH LEADING NEUROLOGICAL 

SYMPTOMS. 

Alcoholism qcq 

The opium and kindred habits ofo 

Tetanus q^c 

Hydrophobia 053 

Arthritis deformans q5q 

Other toxaemic troubles q 7I 



SECTION A. 



INTRODUCTION. 



GENERAL CONSIDERATIONS UPON THE PECULIARITIES 
OF THE NERVOUS SYSTEM AND ITS DISEASES. 

The Nervous System is a unique and complex apparatus for the 
performance of unique and complex functions. Neither its anatomy nor 
its physiology is like that of any other organ of the body. When rough- 
ly contemplated as a mass of tissue, constituting the center, as it were* 
of the entire organism, it has more or less of a uniformity of structure 
and a singleness of function. When regarded minutely in its multitu- 
dinous relations to all the various parts of the body, it is a very com- 
plex, compound organ with a large variety of functions. 

Nervous matter per se consists of a single element and its support- 
ing environment immensely multiplied. The two functions of this ele- 
ment are self-nutrition and the manifestation of a special form of irrita- 
bility. 

A study of nervous matter, whether found in the brain, the spinal 
cord or the peripheral nerves, exhausts itself when the nervous cell 
with its' processes is analyzed. Its functions are summed up in the two 
words, self-nutrition and irritability. Its supporting environment of 
neuroglia, connective tissue and blood vessels is, strictly speaking, extra 
neural, or at least is not primarily involved in the manifestations of 
neurility. 

From this point of view the nervous system is a very simple affair. 
It is a point of view to keep always in mind, for in certain congenital 
diseases, inherited defects and degenerative, systemic maladies it offers 
the only clear explanation. 

It is difficult for us to keep this simple, uniform conception of the 
nervous apparatus clearly before the mind's eye, because we are accus- 
tomed to seemg its activities manifested in so many different ways. 
Mental, motor, sensory, trophic are the ways in which we usually re- 
mark the exhibitions of nerve force. A moment's thought, however, 
will bring home the fact that motion, sensation, mentality, nutrition are 
not nervous phenomena. Motion belongs to the muscles, sensation to 
particular end-organs, nutrition to special embryonic cells and men- 
tality to the interplay of various different processes. In other words, 
the great variety of outward presentations of nervous activity is due 
not to any variety in the structures and functions of the intrinsic nervous 



l8 GENERAL CONSIDERATIONS UPON NERVOUS DISEASES 

elements themselves, but to the different organs and tissues of the body 
with which they are in intimate relationship and which they bind to- 
gether in perfect harmony of action. 

This also is a most important point of view from which to contem- 
plate the nervous system and one which emphasizes the peculiar differ- 
ence between it and the other organs of the body. In the localization 
of the lesion this point of view from which to regard the entire nervous 
apparatus and its functions is a very important one. 

From these standpoints it must be obvious to the casual reader 
even that a thorough knowledge of the histology and physiology both 
of the nervous elements themselves and of the nervous elements with 
their various connections and end-organs must be presupposed before 
any profitable advance can be made in the study of nervous diseases. 
This, of course, is largely true of all the organs and tissues of the body, 
but nowhere in the whole range of medicine, except in neurology, is a 
perfect knowledge of normal structure, normal relationships and normal 
functions so absolutely necessary for the accurate appreciation of ab- 
normal changes and abnormal manifestations. 

The oft-quoted aphorism that disease is nothing but perverted 
physiology comes more nearly to expressing the whole truth in neu- 
rology than in any other department of medicine. Much of the pessi- 
mism, lack of interest and ignorance in regard to the diseases of the 
nervous system spring out of unfamiliarity with the anatomy and 
physiology of the normal nervous system. 

In many other diseases of the body there are new secretions formed, 
new sounds produced, new appearances presented that enable one to 
form a diagnosis along with the aid of a good memory. For example, 
an ascitic fluid, a valvular bruit, a crepitant rale, a peculiar intestinal 
discharge may be so remote from all normal physiological exhibitions 
that its existence alone will quite determine the diagnosis. These un- 
physiological symptoms afford to the examiner a most ready and avail- 
able means of diagnosing disease. 

On the other hand, there is not a symptom belonging to disease of 
the nervous system that is not in its last analysis a simple perversion of 
a physiological manifestation. Fagge was therefore right when long 
ago he declared that the symptoms of nervous disease were almost 
without exception those of perverted nervous function. They reveal 
themselves always as an increase, a diminution or a modification of 
what would be a normal nervous exhibition. 

This is a most important fundamental fact to grasp in beginning 
the study of these diseases. It emphasizes the truth that a clear con- 
ception of the normal anatomy and physiology of the entire apparatus 
is an absolute prerequisite to the further comprehension of its pathology 
and symptomatology. 

Another peculiarity in regard to the nervous system is that most 
of its external manifestations are secondary in character and extraneu- 
ral. At no point except at the fundus of the eye do we at any time 
obtain a direct view of normal, functionating nerve tissue. Hidden 
behind the other organs and tissues, it reveals its own changes of activ- 
ity by the changes of activity in these organs and tissues. Motor, 



GENERAL CONSIDERATIONS UPON NERVOUS DISEASES 10 

vasomotor, sensory and trophic disturbances may all be directly due 
to nervous disturbances, but all that we can observe are the functional 
disturbances of muscles, blood vessels and special cutaneous end-organs 
and the nutritional changes in the related tissues. Occasionally we can 
observe changes in the cptic nerve at the fundus of the eye to corre- 
spond with changes in the vision, but more often even visual dis- 
turbances occur without any discoverable alterations in the fundus. 
Practically all objective nervous manifestations therefore are extraneu- 
ral in character. 

We can only infer corresponding changes in the nervous matter 
from the changes that we see in the non-nervous. Even mental and 
subjective symptoms are practically non-neural in their manifestation. 
The changes in the mental functions are recognized only by the indi- 
vidual himself as being related to motion and sensation. A change of 
volition, for instance, is to the subject himself a conceptual change 
of muscular movement ; an alteration of some, special or general sensa- 
tion is identified with the actual or conceptual alteration in the activity 
of some special end-organ such as the eye, ear or skin. 

Practically, therefore, all nervous manifestations, whether subjec- 
tive or objective, are secondary in character and involve extraneural 
tissues and organs. 

This is a startling and peculiar fact to remember always in con- 
sidering the semeiology of nervous diseases. 

So far as we know, irritability and self-nutrition are the only pri- 
mary physiological manifestations of unrelated nervous matter. When 
we speak of motor, sensory and trophic symptoms we refer merely to 
secondary, extraneural phenomena. Our analysis of the nervous activ- 
ity involves only inference and indirect reasoning. 

There is a third peculiarity in regard to the nervous apparatus that 
must be noted by one who wishes to understand its diseases. Though 
we often speak of it as a single apparatus, and though all its parts usu- 
ally functionate together in harmony, it is really a most complex and 
compound organ, made up of a great conglomeration of little organs 
or deposits of nervous matter, each having its own little sphere of 
activity and each exercising different functions according to the particu- 
lar end-organ with which it happens to be in connection. In the brain, 
in the spinal cord and in the nerves are clumps of elements which sub- 
serve motor, sensory and other functions, and yet lie in the closest sort 
of juxtaposition. 

Many observations in connection with the systemic diseases, with 
the progressive degenerations, and with the changes that sometimes take 
place in widely separated but functionally similar parts of the nervous 
system, lead us to suspect that the nervous elements are not all exactly 
alike in structure. \\ nether they differ chemically, physically or func- 
tionally we cannot guess. That they differ at all is only a matter of 
inference. So far as our present means of examination lead us, we can 
merely say that in structure the nervous system seems to be the same 
everywhere, though in function it is like a multicolored kaleidoscope. 
Xo other organ in the body is thus constructed. As a consequence the 
localization of disease in the nervous svstem is a characteristic and 



20 GENERAL CONSIDERATIONS UPON NERVOUS DISEASES 

diagnostic feature. The same lesion in different parts creates very dif- 
ferent clinical pictures, and the mystery of the so-called selective action 
of poisons and disease processes is in part dissolved. 

Viewed independently, then, the nervous organism is seen to fall 
into a category of its own. Under the impulse of a strong ancestral 
and biological influence it appears in the embryo. The continuation of 
this same prenatal or hereditary influence, coupled later on with an 
environmental and postnatal force, guides and directs its further de- 
velopments. In structure it is made up of innumerable elements whose 
chief powers seem to be functionally those of self-nourishment and the 
exhibition of a high degree of irritability. 

Such is the nervous system apart from all its structural and func- 
tional connections. It represents a mass of protoplasmic cells evolved 
from primitive embryonic cells and differentiated to a high degree for 
the performance of special purposes in the organism at large. It is 
always well to keep this conception of the nervous apparatus in mind, 
for it makes easy of comprehension some of the remarkable things that 
are observed in the nervous system in connection with heredity, de- 
generative influences, general infections and special diseases. 

As a matter of fact, however, the nervous apparatus is practically 
never an independent and unrelated organ. We have already seen how 
it is so intimately associated with the other organs and tissues of the 
body that its own changes of action can only betray themselves by cor- 
responding changes of action in these other organs and tissues. So 
close is the connection and so mutually dependent upon each other are 
the nervous elements and the rest of the organic tissues that the latter 
can even react upon the former almost as vigorously as the former can 
upon the latter. Nervous lesions can produce muscular atrophy ; but 
muscular disease often reacts in a way to cause wasting of the nervous 
elements. Optic atrophy causes the visual organ to undergo marked 
changes, while permanent shutting out of light from the eye results in 
a wasting of the optic nerve. This phrase mens sana in corpora sano 
is expressive of the truth that even mental and physical processes are 
mutually interdependent. 

If the nervous apparatus consists essentially, as I have previously 
indicated, of a mass of highly differentiated cells, it is subject not only 
to the tissues and organs with which these cells are functionally con- 
nected, but also to the tissues and organs which surround and support 
them. The latter, as we know, consist of neuroglia, connective tissue, 
lymphatics and blood vessels. These, together with the nervous ele- 
ments, make up what in gross anatomy is called the nervous system. 
Sometimes the nerve cells are spoken of as the noble and parenchy- 
matous elements, while the nutritive and sustentacula r structures that 
surround them are referred to as the ignoble or interstitial. 

A large number of diseases of the nervous system originate in these 
sustentacular tissues and secondarily damage the nervous apparatus in 
their way, just as diseases of the functionally related organs and tis- 
sues do in theirs. These diseases are literally as much extraneural as 
if they were located in the surrounding bones or membranes. The 
only primary diseases of the nervous apparatus are those that originate 



GENERAL CONSIDERATIONS UPON NERVOUS DISEASES 21 

and have their primary seat in the noble or true elements ; all others 
are secondary. 

The terms primary and secondary used to be employed in a grosser 
sense, the former being applied to all diseases that originated in the 
nervous system as distinguished from diseases that began in the bones, 
membranes and other coarse structures in the neighborhood. 

From the histopathological standpoint only the primary diseases 
of the nervous system are the parenchymatous diseases. The vascular 
and interstitial diseases are literally as much outside of the nervous 
apparatus as would be, for instance, disease of the spinal, vertebral or 
cerebral membranes. They affect the nervous apparatus secondarily 
and cause the appearance of nervous symptoms by their pressure or 
destructive influence upon the parenchymatous elements. Locomotor 
ataxia is a primary nervous disease ; cerebral syphilis of the gummatous 
type is not a nervous disease, but a disease of the blood vessels. The 
nervous changes in the latter are all secondary. 

For the proper appreciation of the intraneural diseases and the 
extraneural this conception of their primary and secondary charac- 
teristics should be insisted upon. Etiologically, pathologically, symp- 
tomatically and therapeutically there is the widest difference between 
the two sets of affections. 

The primary diseases are more subject to hereditary influences than 
are the secondary. They are degenerative in nature and are usually 
provoked by toxic, infective, cachectic, nutritional and other depressing 
causes of a general character. Their symptomatology is purely neu- 
rotic and as a rule is more or less uniform and progressive from the 
start. The localization symptoms are comparatively clear and well de- 
fined. Their prognosis is generally fair as to life, but bad as to recov- 
ery. Their treatment is most discouraging. They are both organic and 
functional, inherited and acquired. Inherited defect is at the bottom 
of a good many of them and accounts largely for the unsatisfactory 
character of their treatment. 

The secondary diseases are the result of traumata and various 
noxious agents. Heredity plays but an insignificant role here. The 
primary seat of these troubles is strictly extraneural, and hence the 
lesions represent all sorts of general and specific vascular and connec- 
tive tissue changes. 

Inflammation is at the foundation of most of these troubles and by 
pressure and otherwise the inflammatory process damages the parenchy- 
matous elements or the true nervous apparatus. 

The symptomatology of these diseases bears a double countenance 
— namely, the symptoms of the vascular disturbance and the symptoms 
of the nervous. The former are varied in character, are more or less 
febrile and are the same wherever the lesion may be located ; the latter 
are more uniform, reveal progressive irritation and destruction of the 
neighboring nerve elements, and are varied according to the location 
of the lesion. As these diseases are usually diffuse, the localization of 
the lesion is not a prominent feature and is possible only when the lesion 
happens to be of a certain character. 

The prognosis of these diseases depends upon the extent of the 



22 GENERAL CONSIDERATIONS UPON NERVOUS DISEASES 

damage done to the nervous elements and to some few particular in- 
herent features of their own. As a rule it is hopeful. 

Their treatment is generally effective and sometimes is rewarded 
with most brilliant success. They are practically all organic diseases, 
though the nervous elements for a time may be only functionally dis- 
turbed. The minimum of influential heredity amongst them accounts 
very largely for their more hopeful management. 

As illustrative of what is meant by primary nervous diseases may 
be mentioned tabes, Friedreich's ataxia, primary Little's disease, some 
types of progressive muscular atrophy, amyotrophic lateral sclerosis, 
progressive bulbar paralysis and most of the so-called neuroses. 

Among the secondary group I would place all of the inflammations, 
hemorrhages, neoplasms, and vascular, connective tissue changes, 
whether they occur in the tissues immediately surrounding the nervous 
elements or in the more remote membranes, bones, etc. Myelitis, en- 
cephalitis and neuritis occur here. All forms of vascular diseases, such 
as arteritis, hemorrhage, embolism, thrombosis, must be included. 
Tumors are all extraneural primarily, even including the unique glio- 
mata. Primary sclerotic processes are extraneural, being due to con- 
nective tissue changes. It hardly needs to be mentioned that diseases 
of the meninges and of the osseous coverings are pre-eminently extra- 
neural. 

These illustrations of what is meant by primary and secondary 
nervous diseases do not include all of the known affections by any 
means. The principle underlying the distinction having once been rec- 
ognized, it will be an easy matter when the diseases are studied in detail 
to assign them respectively to one or the other class as we learn their 
pathology. 

The Classification of the diseases of the. nervous system is still 
in a most chaotic condition. There is an obvious reason for this. Hith- 
erto all tlassifications have been based upon such varied and hetero- 
geneous factors as gross, arbitrary anatomical subdivisions, upon par- 
ticularly prominent symptoms, or upon strange etiological and thera- 
peutical distinctions. Some of these classifications were so absurd that 
they have long passed into the limbo of oblivion. Our knowledge of the 
nervous system is so incomplete that we still find justification for the 
calling of a special symptom a disease and giving it all the dignity of a 
special chapter. Though we no longer head a page in our modern text- 
books with such meaningless terms as paralysis and apoplexy, we still 
treat chorea and hydrocephalus and hemicrania and headache and 
vertigo as though they were diseases. By the later elimination of the 
names Landry's Paralysis, Meniere's Disease and others and the proper 
assignment of these diseases to the places which their pathology indi- 
cates, it is seen that we are steadily though slowly progressing towards 
a more accurate neurological nosology. Some day symptoms will not be 
employed at all as the basis of classification. 

It was long ago recognized that the pathology of a disease should 
constitute the only guide for its name and classification. Pathology, 
however, involves both the location and the character of the lesion. 
Many authors adopt both factors in their classification. In one pah of 



GENERAL CONSIDERATIONS UPON NERVOUS DISEASES 23 

the book will be found the discussion of the system diseases. Here the 
location of the lesion is the prominent feature. In another part of the 
book there will be found a discussion of tumors of the nervous system 
and syphilis. Here obviously the character of the lesion is the principal 
consideration. It must be frankly admitted that in the present state of 
our knowledge such incongruity is not altogether blameworthy. In 
fact, it has its advantages for the present. Some clay, however, this 
also will be avoidable. 

A very gross, yet convenient, classification, based upon location, is 
that which divides the diseases into those of the brain, spinal cord and 
peripheral nerves. Modern histology, and especially its recent magnifi- 
cent generalization, the Neurone Doctrine, has demonstrated that it is 
coarse and arbitrary to divide the nervous system into brain, spinal 
cord and nerves. It has shown us that there are no lines of separation 
between these so-called parts of the nervous system. Processes from 
the brain cells pass far into the cord from above, while processes from 
the nerves extend high up into it from below. From the cord cells pass, 
in opposite directions, processes into the brain above and into the nerves 
below. In other words, most of the nervous elements lie partly in one 
and partly in another of these so-called divisions of the nervous system. 
Our ignorance of this fact has hitherto caused some most erroneous 
conceptions and classifications of the nervous affections and the incubus 
of it we even yet find hard to shake off. We still sometimes refer to 
locomotor ataxia as a spinal cord disease, though its lesion is chiefly 
found in nervous elements that extend farther outside of than inside of 
the spinal canal. There are certain bulbar diseases that present a symp- 
tomatology more nearly related to spinal cord than to brain phenomena. 
It is a question in the minds of some pathologists whether certain forms 
of so-called peripheral neuritis are not really degenerative processes in 
the peripheral nerves due to trophic disturbances in the anterior horns of 
the cord. Certain eye symptoms have long been recognized as attrib- 
utable to disease in the lower part of the cervical cord. 

So far as the tracts and cellular processes are concerned in diseases 
of the nervous system, there are no demarkation lines between the brain, 
cord and peripheral nerves. As we will see when we come to discuss 
the neurone and neurone theory, the diseases that attack the true 
nervous elements primarily, the true nervous diseases, extend from 
brain into cord and into nerves and vice versa. They do not confine 
themselves to any one of these arbitrary divisions of the anatomists, 
but follow the course of the nervous elements. They may be classified, 
therefore, as Neuronic Diseases. They are the most truly nervous of all 
the nervous diseases. They are organic and functional, the former be- 
ing quite sharply localized, the latter being more diffuse and including 
to a large extent the so-called Neuroses and Psychoneuroses. 

The Neuronic Diseases and the Neuroses, therefore, will be treated 
of in sections by themselves and no attempt will be made to classify 
them as brain, cord or peripheral nerve affections. 

An examination of the gray matter of the nervous system reveals 
the fact that it is made up of a series of aggregations of cells extending 
all along the cerebro-spinal canal. These ganglia, or little brains, as it 



24 GENERAL CONSIDERATIONS UPON NERVOUS DISEASES 

were, are to a certain extent independent in their individual activities 
and control without much interference various related organs and parts 
of the body. These ganglia are numerous and are found everywhere, 
though regularly situated in all parts of the nervous system. They are 
in the sympathetic system, in the posterior spinal roots, and in many 
of the cranial nerves. They constitute the central gray matter of the 
cord as explained in the chapter on die minute anatomy of the cord. 
They are found in the nuclei, basal ganglia and cortex of the brain. 
Since their functions differ on account of their connection with differ- 
ent end-organs and different parts of the body, when they are anywhere 
attacked by disease, the location of the lesion can be at once determined 
by the peculiar symptoms presented. When the intraspinal ganglia, 
for instance, are affected, the symptoms are quite different from what 
they are when any of the intracranial ganglia are implicated. There- 
fore, for obvious reasons, we still find it convenient to speak of dis- 
eases of the brain, of the cord, of the nerves and of the sympathetic 
system. 

In each of these divisions there are many distinct ganglionic masses 
with sharply defined functions. This enables us to carry the classifica- 
tion of diseases on the basis of location to a still higher point. \\ e 
subdivide those of the brain, for instance, into those of the cerebrum, 
the cerebellum, the pons and the medulla. We might carry the division 
even still farther, but as a matter of fact do not find it specially con- 
venient to do so. We might even speak of the diseases of the motor 
cortex, of the visual cortex, of the sensory cortex, of the cervical cord, 
of the lumbar cord, etc. All this, however, can better be left to the con- 
sideration of the cerebral and spinal localizations in the chapters devoted 
to the anatomy of the brain and cord. 

In the following work I will adopt this provisional classification of 
the diseases of the nervous system, believing it to be justified by the 
present state of our knowledge, and realizing perfectly that newer dis- 
coveries will from time to time transfer some of the diseases from one 
group into another. 

Neuronic Diseases. 

(Parenchymatous Degenerative Troubles.) 

a. The Functional Neuronic Diseases. 

i. Cerebro-spinal. 
2. Sympathetic. 

b. The Organic Neuronic Diseases. 

i. Of the Afferent System. 

2. Of the Efferent System. 

3. Of Both the Afferent and Efferent Systems. 
Non-Neuronic Diseases. 

(Interstitial and Vascular troubles affecting the Neurones 
secondarily.) 

a. Of the Spinal Cord and its Membranes. 

b. Of the Peripheral Nerves. 

c. Of the Brain and its Membranes. 

General Intoxications with Special Nervous Symptoms* 



GENERAL CONSIDERATIONS UPON NERVOUS DISEASES 



GENERAL CONSIDERATIONS UPON THE ETIOLOGY OF 
DISEASES OF THE NERVOUS SYSTEM. 

It is premature to formulate an exact etiology or classification of 
the causes of diseases of the nervous system. They are so many, so 
varied and so indistinct sometimes that we are quite at a loss to give 
to them always their deserved valuation. 

For many reasons, however, an attempt should be made to gener- 
alize, so far as known data will warrant, the etiology of these affections. 

In the first place, the causation lying behind the pathology serves 
as the guide to the proper therapy. Our management of these dis- 
eases, even more so than in others, cannot proceed along logical 
and scientific lines as to the best interests of the patient until we have 
a clear conception of their etiology and pathology. It seems like a 
truism to say this and yet the pre-eminence given to therapeutics, to the 
neglect of etiology and pathology, is the folly of the quack, the ignor- 
ance of the layman and the weakness of the physician. 

In the second place, we are so rapidly eliminating the innumer- 
able causative factors harped upon by the writers of the past, and 
discovering so much more positively the comparatively few real causes, 
that the time is getting ripe for an attempt at a systematic arrange- 
ment of the latter. 

In the third place, our knowledge of the pathology of nervous 
diseases has lately grown so and our conception of its relationship to 
all etiological antecedents has clarified to such a degree, that we are 
beginning to occupy a position to speak with a high tone of positive- 
ness of the latter as being the undeniable causes. 

In the fourth place, a study of the etiology of these affections 
points out a line for the classification of the diseases themselves, enables 
us to calculate the possibility of the removal of the cause and of the 
disease, and helps to determine the prognosis as well as the hopeful- 
ness or hopelessness of treatment. 

As all diseases of the nervous system naturally fall into one or 
the other of the two groups — namely, those that start primarily in the 
neurones and those that start primarily outside of the neurones, we 
must remember this in studying their etiology, for the latter is not 
exactly the same in all particulars for both. This will be noticed as 
we proceed in the discussion of the causes and especially when the 
particular diseases themselves are taken up for consideration. 

Another useful, because practical, division of the causation of 
nervous diseases is into those that are endogenous or developed within 
the body, and those that are exogenous or exert their influence from 
without. 

An anaemia is an endogenous cause of nervous degeneracy ; a blow 
on the head is an exogenous cause of meningitis. 

It would be perhaps too fine a distinction to speak of the endogen- 
ous and exogenous causes in relation to the neurones or true nervous 
elements; and yet such a division would be both scientific and prac- 
tical, for all of the hereditary diseases are practically due to endogenous 



26 GENERAL CONSIDERATIONS UPON XLPVOUS DISEASES 

influences within the neurones, while all other diseases, whether merely 
congenital or prenatal, natal or postnatal, are exogenous. 

A grand starting point for the study of the etiology of nervous 
diseases is the division of the causes into the predisposing and the 
exciting. The former are inherent, of course, and include everything 
that involves the patient's individual body and personality. They there- 
fore take cognizance of his heredity, his intrauterine development, his 
birth and his constitutional state and his subjection to other diseases 
up to the moment of examination. They are concerned with his age, 
sex, nationality, occupation, mode of life and habits, his climatic, 
hygienic and social environment. The exciting causes are not neces- 
sarily inherent in the patient. As a matter of fact, they are more fre- 
quently external, all more or less temporary, and invade an organism 
rather abruptly. They include the traumata, the intoxications and the 
infections. Among the reflex causes so much referred to by many 
writers, some are of the nature of mere predisposing factors, some fall 
into the category of direct traumata. I will discuss them later on. 

For convenience we may formulate the following scheme /)f the 
causes of the diseases of the nervous system : 

1. Predisposing causes. 

Heredity. 

Age. 

Sex. 

Nationality. 

Occupation. 

Mode of Life and Habits. 

Climatic, Hygienic and Social Environment. 

2. Exciting causes. 

Traumata. 

Intoxications. 

Infections. 

3. Reflex causes. 

I will now discuss these a little more in detail and explain the 
omission in the schema grossly outlined above, some causes, as, for 
instance, tumors, parasites, etc. 

As has been long recognized, heredity plays its most brilliant role 
in connection with the nervous tissues. So recently has the nervous 
system, at least in its highest and most complex elaboration, been 
evolved in the course of biological development that we can trace an- 
cestral phenomena, both anatomical and functional, better in it than 
in any other organ or tissue of the body. Zoologists recognize this so 
forcibly that they arc beginning to use the nervous apparatus for the 
basis of their higher classifications and to trace out with its aid the 
lines of descent in the various classes of animals. In neurology we 
have come to acknowledge that heredity is the most important factor 
biologically for modifying the nervous apparatus for good or for evil. 
Note carefully here the use of terms. I snid the nervous apparatus. 
Strictly speaking, this includes, we now know, only the neurones and 
the neuroglia. Tt follows logically and it is clearly demonstrated em- 



GENERAL CONSIDERATIONS UPON NERVOUS DISEASES 2J 

pirically, that in the neuronic and neurogliomatous diseases only do we 
find heredity exerting the most transcendent force. Many of the dis- 
eases of this class are purely and entirely hereditary. They are of 
the nature of inherited defects. Such, for example, are Friedreich's 
disease, some of the progressive muscular atrophies, the so-called con- 
genital neurasthenias, hysterias, epilepsies. 

There are other diseases of the neuronic class, however, that are 
provoked into existence by one or more exciting causes, but are local- 
ized and otherwise determined by the patient's heredity. In these there 
is a tendency toward the disease, but it remains latent until some ex- 
traneous cause starts the latent influence into action. It is believed 
that this explanation applies to many of the acquired systemic diseases 
like locomotor ataxia, to most of the gliomatous conditions and to a 
large number of the acquired and secondary neurasthenias, hysterias, 
-epilepsies and other so-called functional neuroses. It is going too far, 
however, to affirm, as some have done, that a true neuronic disease 
cannot develop, whatever the exciting cause may be, unless there is 
an inherited neuropathic weakness of some sort present. It is not at 
all improbable that monotonous overexertion, intoxication or infection 
may expose itself in a disease of neurones that may originally have been 
endowed with perfect health. These cases, however, are not as com- 
mon as is generally supposed. It is astonishing the amount of strain 
the perfectly healthy and well-developed nervous apparatus will bear. 
Most of the breakdowns that we observe in actual life, whether of the 
organic or functional type of neuronic disease, owe a large part, of 
their misfortune to the inheritance of an inadequate strength and 
vitality. 

In the diseases that start outside of the neurones heredity plays 
such a small part that it amounts to practically nothing. In certain 
vascular troubles, such as the cerebral hemorrhages and possibly in 
some of the tumors, there is a bare trace of hereditary influence. In 
the traumatic, toxic and infectious troubles that cause inflammation 
and all its sequelae, it is practically nil. The diseases that occur as 
the result of hereditary syphilis are not hereditary nervous diseases. 
Hence what I will say in regard to heredity will apply more particu- 
larly to the neuronic degenerations and neuroses. 

By direct heredity is meant the transmission of the same disease 
from parent to child. Such heredity is not common. More frequently 
a nervous weakness or tendency is handed down. This is known as 
indirect heredity. When the hereditary influence is towards the pro- 
duction of the same disease in the child that was in the parent, it is 
spoken of as an inherited tendency. Even this is not so common. 
Much more frequently the progeny is presented with a neuropathic 
taint merely, which, upon provocation or without, may develop a simi- 
lar or dissimilar disease from that observed in the ancestry. A neu- 
ropathic diathesis is so frequently traceable in these cases that no ex- 
amination is properly conducted in which it is not promptly and most 
persistently inquired into. 

It is not always necessary that there should be a well-defined dis- 
ease in the parentage. Nervous strain may be sufficient to cause the 



28 GENERAL CONSIDERATIONS UPON XERVOUS DISEASES 

children to inherit a constitution that soon revels in the most elaborate 
forms of nervous disease. I have seen a girl go insane with a primary 
form of degenerative dementia for which no other possible cause could 
be detected than a congenital neuropathic weakness. When she was 
conceived and being carried her mother was under excessive worry 
and a physical and mental strain striving to make a living for a large 
and healthfully growing family. Hard brain workers, those who dis- 
sipate and indulge freely in alcohol and tobacco, often transmit to their 
children a vitiated nervous apparatus. The latter surfer from neu- 
rasthenia, hysteria, epilepsy and various psychoses. If both parents are 
neurotic or subject themselves to causes that deteriorate the nervous 
system, the chances for the children are bad. The intermarriage of 
blood relatives is dangerous for the offspring. I have under observa- 
tion now a middle-aged man, the father of two vigorous, grown-up 
daughters, who has been the victim during the last eight years of 
typical disseminated sclerosis. His habits have always been exemplary 
and there is no known exciting cause for the disease. His paternal 
grandparents, however, were first cousins. His own father and a 
paternal uncle and aunt were all congenital deaf mutes. His own 
mother became a deaf mute from scarlet fever in childhood. The pa- 
tient himself ts the younger and weaker of twins. 

Mental troubles not infrequently follow close blood intermarriages^ 
Dean concludes from his examination of 181 cases of eye troubles in an 
institution for the blind that of the congenital cases fourteen per cent 
were the result of consanguineous marriages of the first degree. He- 
believes from his statistics that the greater the inheritability of a con- 
dition the more liable it is to be the result of consanguineous marriage. 

Sometimes the parent will be afflicted with a typical disease while 
the child will reveal only a general neuropathic depreciation. A mother 
is epileptic, her daughter becomes hysterical. It may be vice versa 
A father has all his life had attacks of typical hemicrania ; his child has 
epileptic fits or becomes the victim of dementia prsecox. Chorea breaks 
out in the children of markedly neurasthenic parents. The neuroses 
are more frequently transmitted by the mother than by the father. 

The heredity has been seen to be direct, if I may say so, in alter- 
nate generations, indirect in succeeding generations. Epilepsy, for 
instance, has been among the grandparents ; genius with some of its 
oddities and psychic peculiarities appeared in the next generation ; 
epilepsy again, with terminal insanity, reappear in the third genera- 
tion. This is sometimes called a manifestation of atavism, a reversal 
to earlier forms of nervous exhibition. 

Atavism is a remarkable and not such an uncommon phenomenon 
in the animal world. It is not frequent, however, in connection with 
nervous diseases. Indeed, it may seriously be questioned whether the 
mere repetition of the same disease back of the preceding generation 
is a true form of atavism. A disease in the ancestor is not necessarily 
an earlier or more primitive type of that seen in the progeny. It is 
really the same disease probably occurring in the same sort of a neu- 
ropathic constitution. As a phenomenon, however, this atavistic ten- 
dency in nervous disease, whether real or apparent, is interesting and 



GENERAL CONSIDERATIONS UPON NERVOUS DISEASES 29 

^worthy of further study. The same may be said of those diseases that 
sometimes appear in collateral branches or in several members of the 
same family, so that they are spoken of as "familial diseases." These 
are largely of the nature of developmental defects or anomalies. Fried- 
reich's disease and some of the atrophies may be cited as illustrations. 
Glioma is a congenital defect. Diseases that reappear, and the morbid 
conditions that occur, later in life in the descendants than they did in 
the ancestry, may be looked upon as waning in the family. 

Under the head of heredity the modern doctrines of degeneracy 
must receive some consideration. The term is one that is much abused 
and misunderstood. 

Degeneracy is the result of a biological taint. It is a product of 
hereditary and congenital influences. It is not the immediate result of 
environment. It therefore does not mean a falling back of the individ- 
ual from a previously normal state, but a falling back of the racial or 
familial development, as shown in the anomalous and primitive stigmata 
of the individual. A degenerate is what he is because of his ancestry, 
and not because of anything he himself has done. It is therefore a 
misfortune, not a disgrace. In the physical sphere it shows itself by 
various stigmata, the value of which have not all been positively estab- 
lished. No man is perfect physically and yet we do not consider all 
men as degenerates. Just where degeneracy stops and so-called nor- 
mality begins is a hazy region ;- hence the many extreme and ofttimes 
absurd notions put forth by those who believe and those who reject 
the doctrines of Lombroso. Asymmetry of the skull, protrusion of the 
lower teeth, irregularities about the eyes, anomalies in connection with 
the ears, disproportion between different parts of the face are all often 
signs of physical imperfection. Still greater degeneracy is seen in 
such conditions as hare-lip, cleft palate, irregular teeth, retinitis pig- 
mentosa, albinism perhaps. And yet too much must not be inferred 
even from such coarse defects as these. Most epileptics reveal more or 
less stigmata of degeneracy. Cranks and queer people very often pos- 
sess them. Genius has been accompanied by them. On the street 
scarcely an individual is seen who does not exhibit some similar phys- 
ical anomaly in greater or less degree. -» 

There are parallel stigmata in the neurotic and psychic manifesta- 
tions. They may range all the way from a slight eccentricity of thought 
and manner down to gross mental debility, imbecility and idiocy. As 
no man is perfect physically, so no man is perfect mentally. 

This is all too obvious when a definition of what is meant by nor- 
mal mentality is attempted in court during a trial for insanity. So 
many factors enter into the make-up of one's mental manifestations 
that what is craziness in one man is perfect mentality in another. The 
points of view vary. Hottentots are not insane, nor even degenerate, 
because they do not think and act as Englishmen do. A genius, an 
artist, may well appear to be erratic, even crazy, beside a dull financier 
with his one idea of money-getting. Their opinions of each other in 
regard to their mental exhibitions will probably be mutually uncom- 
plimentary. 

We may, if we please, call the average man normal. Only in 



30 GENERAL CONSIDERATIONS UPON NERVOUS DISEASES 

comparatively coarse defects, however, can the positively abnormal be 
recognized. Genius is eccentric, even crazy at times ; so seems the 
dull monotony occasionally of the average man. 

It behooves the true scientist to be conservative in his conceptions- 
of mental and nervous degeneracy, just as he must be conservative in 
deciding who are afflicted with the stigmata of physical degeneracy. 

Along coarse lines we can recognize both psychic and physical de- 
generacy. We can even note a remarkable parallelism running be- 
tween them. A wholesale slashing about of the doctrine as some en- 
thusiasts have made, attributing degeneracy to all geniuses and bril- 
liant intellects, and to all deviations from their preconceived notions of 
physical and mental perfection, will lead, in the present state of our 
knowledge, like a boomerang, back to their own imperfections and de- 
generate reasonings. 

The age of the individual exercises a considerable influence in 
determining the nature of the disease. This is partly on account of the 
differences in the patient's own organism and in his habits and en- 
vironment in different years. It may even be entirely secondary so 
far as the nervous system itself is concerned, for the primary disease 
may entirely determine the age at which the nervous troubles appear. 
The nervous sequelae of scarlet fever, for instance, occur in childhood 
merely because scarlet fever is a childhood disease. In childhood and 
early life generally the congenital troubles that result from prenatal and 
natal injuries usually declare themselves. Hereditary troubles also are 
apt to appear early. The infectious fevers that occur in children are 
responsible for a large number of nervous diseases. Early malnutrition 
exerts its influence, as well as unwonted strains. The child's nervous 
apparatus is, of course, a growing and immature one, a fact which 
exercises some force in the determination of the kind of disease, as 
well as of its symptomatology and prognosis. 

In middle and later childhood we observe a predominance of motor 
troubles, such as chorea, paralysis and convulsive seizures. The ex- 
cessive use of the motor apparatus in learning to talk, to walk and to 
adjust the young creature to his environment is possibly the cause of 
this. 

About the time of puberty the sensory and emotional disorders are 
in the ascendent. Under the awakening of the sexual life and all that 
it means both in the individual's inner sensibilities and in his relation- 
ship to his surroundings, hysteria, neurasthenia, epilepsy, sleep troubles, 
hypochondriasis and inherited tendencies, nervous and mental, are apt 
to break out. 

From puberty on to the climacteric the nervous system is more « r 
less stationary and developed, but it is subjected to all of the strains of 
an active adult life. Traumatisms of all sorts now come into play. So 
do the intoxications and infectious diseases of adults. 

After the climacteric the troubles of old age, the degenerations of 
all the tissues, nervous and vascular, are to be counted upon. Hence 
the senile weakness, the apoplexies, the softenings, the arteriosclerotic 
and atheromatous degenerations, vertigos, neuralgias and paralyses are 
common. 



GENERAL CONSIDERATIONS UPON NERVOUS DISEASES 31 

The influence of sex is a knotty question. Women are more emo- 
tional than men and are undoubtedly subject to different physiological 
influences. But they also lead very different lives from men. The 
neuroses and sensory disorders predominate among them, whereas the 
organic and motor affections lead among men. Just how much of this 
is to be attributed to their difference of organization, and how much 
to their difference of mode of living, it is not easy to say. More study 
is needed before the influence of sex upon the development of nervous 
disorders can be dogmatically spoken upon, 

Nationality seems to have some bearing. Whether this is a racial, 
a biological or a mere geographical factor is not entirely known. The 
neuroses, for instance, are more prominent among the Jews and the 
Latin races of Europe. They are old races and have been historically 
subjected to most unhappy conditions. A degree of degeneracy there- 
fore may account in part at least for their proneness to the functional 
troubles. The organic diseases are more common in the Germanic and 
Anglo-Saxon peoples. Locomotor ataxia is a rarity in the Negro and 
the Jap. The insanities of childhood are almost considered American 
diseases, but they are probably due to the strenuous lives we live here. 
Certain immigrant races, such as the Bohemians and Poles, probably 
owe their susceptibility to epilepsy and other neuroses to their de- 
pressed conditions in life as much as to their nationality. France is 
the home of hysteria ; as a people the French live a comparatively 
sensuous, unrestrained and highly emotional existence. 

All occupations that are in unhygienic surroundings, that are 
monotonously prolonged, that necessitate irregularity of habits, that 
interfere with sufficient exercise, fresh air and relaxation, that, in a 
word, destroy. the nice balance between all the functions of the body 
necessary for its health, predispose towards the development of nervous 
troubles. Much neurasthenia is attributed to hard work, especially 
mental work, in these strenuous days, whereas it is not the work that 
is to be blamed, but the monotony of it and the one-sided development 
which it enforces. Hysteria is often provoked by the narrow mental 
lives that many women lead, as well as by their want of self-discipline. 

Occupations of some kinds are particularly prone to lead to 
nervous troubles on account of the exposure to accidents, to intoxica- 
tion and to infection. Bridge builders are liable to the caisson disease ; 
saloonkeepers suffer from alcoholic degenerations ; lead workers some- 
times develop lead palsy ; and traveling men get syphilis and develop 
tertiary consequences. 

It is said that the unmarried suffer more from nervous diseases 
than the married. The freer life and greater dissipation of the former 
may be the proper explanation for this. 

The whole subject of occupation, environment and the special 
dangers therein is a large one and can only be referred to briefly here. 

The influence of the mode of life that an individual lives has 
already been hinted at in the consideration of the age, sex, occupation 
and nationality. It is very great. It involves the mental as well as 
the physical life. Overindulgence in eating, in the use of spirituous 
beverages, tea, coffee, tobacco, is a prolific source of nervous trouble. 



$2 GENERAL CONSIDERATIONS UPON NERVOUS DISEASES 

Bad sleeping arrangements, bad bathing customs, bad methods in 
everything will surely lead to misfortune. It is astounding how some 
of the simplest intimations of nature are misinterpreted and unheeded 
by those who ought to know better. A physician, in a high degree an 
irritable neurasthenic, came to me and declared that he did not seem 
to get well, but worse, though he stimulated himself up every day 
with a cold plunge bath in the morning, full doses of strychnia and 
long, exhausting walks. I told him I was not surprised : 

Excessive sexual indulgence is undoubtedly a source of much 
nervous breakdown in both married and unmarried. Athletics and the 
indulgence in outdoor sports at the present time are so excessive that 
they become a source of danger by putting unusual strain upon the 
vascular system. 

On the mental side, sensational literature, narrow thinking and 
the habit of flaring up in anger at every trifle are highly conducive to 
the development of the neuroses, as well as being often a symptom of 
them. Why is it so frequently forgotten that the mind is as much in 
need of proper exercise as the muscles are? The mind is a product of 
brain activity and the brain grows or wastes just as any other tissue 
of the body if it is exercised or neglected. We do not know what parts 
of the brain subserve particular faculties of the mind, but we do know 
that as a sort of counterpart to the biceps and triceps and lumbar mus- 
cles of the body there is a memory and an imagination, a logical and 
a speech faculty. How pitifully lop-sided is that man who toils daily 
after business hours in the gymnasium with his dumbbells and Indian 
clubs in order to develop the muscular system, but who never once 
thinks of exercising specifically his imagination or his memory. The 
dull round of his routine life does not afford the opportunity for very 
wide mental development. 

I am convinced that one-sidedness in mental development as well as 
one-sidedness in physical is responsible for some of the neurasthenia 
and hysteria which we observe about us. 

A volume could be written upon the influence of habits and the 
mode of life in the fostering of nervous affections. 

Climate, apart from mere racial and geographical influences, is not 
an important factor in the etiology of nervous diseases. The fact that 
these are more common in the temperate zones is because there the 
strenuous life and extreme competition are found. This suggests the 
truth that civilization is responsible for much nervous and mental trou- 
ble. Neurologists and alienists would find their services at a discount 
among barbarous races. In the centers where civilization is burning at 
white heat, as it were, namely, the great cities, there the nervous trou- 
bles are in abundance. In fact they are on the increase. The two great- 
est causes of these affections were included in that happy epigram 
of Krafft-Ebing, "syphilization and civilization." We must be careful, 
however, not to charge civilization with what is to be blamed upon squal- 
or and vile conditions in some of our cities. To argue as Rousseau did 
that we need to return to barbarism is a bad mixing up of cause and 
effect, of separate and distinct forces, that is wholly inexcusable. Civi- 
lization in its true sense means culture, refinement, comfort and mental 



GENERAL CONSIDERATIONS UPON NERVOUS DISEASES 33 

elevation. Because ignorance, stupidity, greed and poverty happen to 
loom up where civilization is existent, it merely shows by the contrast 
that much good has been accomplished though much is yet to be ac- 
complished. Not civilization but the abuse of the opportunities offered 
by civilization is the cause of the apparent increase of nervous troubles. 

Among the predisposing causes of nervous affections, certain 
diatheses must not be overlooked, especially the gouty and rheumatic. 
What passes under the general name of the lithaemic condition is read- 
ily recognized clinically, though the nature of the defective process 
is not fully understood. Faulty metabolism with faulty elimination is 
perhaps the real difficulty. How this reacts upon the nervous system 
to produce functional and peripheral diseases is not clear but that it 
does do so is amply demonstrated both clinically and therapeutically. 

I come now to the exciting causes of nervous diseases, and first 
and foremost I place in the list the traumata. These include all kinds 
of physical and mental insults. A terrific blow on the head may pro- 
duce less serious effects than a terrible fright. Bodily injuries of all 
sorts, especially about the head, may set up profound nervous and 
mental deterioration. Primarily or secondarily the delicate neurones 
may be disturbed. From a gross fracture of the skull, all the way 
to a mere concussion, may the traumata range. The former lacerates, 
compresses, invades with hemorrhage, inflammation and infection the 
cerebral tissues; the latter jars and disturbs the functions of the 
neurones in such a way as to give rise to neurosis. Exposure to cold 
and damp is of the nature of a trauma. So are sudden excitement, 
unnatural coitus and many other causes given in the books. 

Almost any form of infection may give rise to disease of the 
nervous organism. Usually it is of the inflammatory type of disease 
though in some chronic infections it may be non-infiammatory and 
purely a neuronic degeneration. It is generally believed that not the 
germs themselves but their toxic products are the immediate causes of 
the disease process. Syphilis, both acute and chronic, acquired and inher- 
ited, is highly blameable. Scarlet fever, measles, influenza, pertussis, 
erysipelas, gonorrhoea, septicaemia, pyaemia, etc., all enter into the etiol- 
ogy of nervous affections. Tuberculosis, near and remote abscesses and 
other germ troubles may provoke metastatic lesions in the nerve cen- 
ters. Some tumors and parasitic growths should probably be classed 
here, though in a way they act more as traumatic causes by compress- 
ing and mechanically irritating the nervous elements near which they 
are located. Until we know more about the pathogenesis of these neo- 
plasms we can only say that infection and traumatism are the imme- 
diate causes of the nervous disturbances when they are present. 

Of the intoxications that provoke nervous maladies, the alcoholic 
far outranks all the others. Lead, arsenic, mercury, aniline, copper, 
carbon dioxide, tea, coffee and tobacco are a few of the intoxicants. 
Here should be mentioned also the drugs that are sometimes used as 
a habit, morphine, cocaine, chloral. Autointoxication together with 
malnutrition is probably the explanation of the etiological bases of the 
various cachexias, of anaemia, of diabetes mellitus, of nephritis and 
certain alimentary troubles. 



34 GENERAL CONSIDERATIONS UPON NERVOUS DISEASES 

Finally, a word must be said upon the much-discussed reflex 
causes of nervous diseases. To deny all etiological influence of a re- 
flex character is to deny the reflex phenomenon of the normal nervous 
apparatus. To attribute disease in the otherwise unaffected nervous 
centers to a mere reflex activity, which is a normal function of a nor- 
mal nervous system, is illogical on the face of it. Therefore, we as- 
sume that a constant reflex excitement of the nervous apparatus pro- 
duces the manifestation of disease symptoms in only one of two condi- 
tions ; either as an excitant to an already abnormal and diseased nervous 
organism or as an excitant to an exhausted and wearied one. 

In the first case the reflex is not the primary cause of the dis- 
ease but is clearly a mere irritant to it. 

In the second case, it may be seriously questioned whether a mere 
state of exhaustion ever becomes transformed into a specific type of 
disease. Let me illustrate. There are ophthalmologists to-day who 
attribute epilepsy to eye-strain. Where there is epilepsy, eye-strain 
as well as a painful corn on the toe, a phimosis or an impacted bowel 
may provoke the attacks. If there is a tendency to epilepsy even, eye- 
strain may start the disease into activity. In all cases of epilepsy 
therefore the eyes should be corrected if need be, but don't charge the 
eyes with the central nervous trouble. When it is contended that eye- 
strain produces epilepsy de novo in a previously healthy nervous appa- 
ratus, it is incumbent upon the ophthalmologist to explain how it does 
it. He declares that it does it by exhausting the nervous centers. He 
has been betrayed clearly in his pathology by the use of the unfortu- 
nate word functional. Epilepsy, hysteria and neurasthenia we may 
grant for argument's sake are all alike in being functional but their 
very symptomatology proves that they are not alike in their origin 
and physical basis wherever and whatever that may be. The eye-strain 
of the ophthalmologists' pathology acts always in the one way, namely, 
as an exhausting strain, and yet strange to say it produces a variety 
of distinct specific diseases of a different character in different indi- 
viduals. 

Knowledge of the pathogenesis of these various diseases is not as 
clear as it should be but it certainly is clear enough to reveal the illog- 
ical reasoning of those who attribute a series of distinct, sharply-de- 
fined, different affections to a mere peripheral wearying reflex that is 
always the same in character and points to no direct connection between 
these various diseases or between them and itself. The causation of 
different distinct pathological conditions in a previously normal system 
by the mere constant exercise of a single and uniform reflex irritation 
is a step backward and brings us face to face again with a pathology 
that is hazy and antiquated and from which we had fondly thought mod- 
ern neurology was redeemed. 

In my opinion, nervous diseases are not reflex diseases though 
they may be aroused into expression, or excited into greater activity 
when so aroused, by a dozen or more sources of peripheral reflex stim- 
ulation. 



GENERAL CONSIDERATIONS UPON NERVOUS DISEASES 35 



GENERAL CONSIDERATIONS UPON THE PATHOLOGY OF 
NERVOUS DISEASES. 

In order to have a clear comprehension of the pathology of the 
diseases of the nervous system, one must keep well in mind the com- 
plex character of the nervous tissues and their relationship to all the 
other tissues. Many diseases are secondary to extraneous affections 
that cause pressure or by extension and metastases invade the nervous 
system. Therefore in these diseases frequently there are pathological 
findings of great importance in other parts of the body. For instance, 
intracranial embolism is usually associated with valvular heart dis- 
ease ; tuberculous meningitis is accompanied by tuberculous foci in the 
lungs; abscess of the brain is very largely due to suppurative otitis 
media; damage to the spinal cord frequently results from caries of 
the spine; disease of the muscles and various end-organs in direct 
functional connection with the neurones not infrequently sets up de- 
generative changes in the latter. 

It is not our province to refer to all of these extraneural troubles 
but merely to the pathological changes which they and other causes 
set up within the nervous apparatus. 

It will be remembered that nervous tissue consists of two dis- 
tinct sets of elements, developed from different embryonic layers in the 
ovum. The true nervous elements are the neurones and the neuroglia 
cells. Though these differ in function, the former being the excitable 
elements while the latter are merely sustentacular or supporting, both 
are found only in the nervous system, and developed from the epiblast 
are non-vascular. 

The false nervous elements are the connective tissue cells, the 
blood vessels, the lymphatics and the epithelium lining the ventricles. 
The function of these is to nourish and furnish a matrix for the true 
nervous elements. They are found in other parts of the body as well 
as here, are mesoblastic in origin and are vascular. 

Pathologically then the nervous system is liable to two great types 
of change. The non-vascular elements undergo degeneration, the vas- 
cular elements undergo inflammation. 

Degeneration is the only change that ever occurs in the neurones. 
The neuroglia cells may proliferate, form tumors and then undergo 
degeneration. 

Inflammation with all its attendant conditions, hemorrhage, vas- 
cular obstruction, infective processes, connective-tissue and parasitic 
new-growths, and sclerotic changes may occur in the vascular con- 
nective-tissue of the nervous system just as they may occur in the 
vascular connective-tissue of other organs and parts of the body. Un- 
der such circumstances the true or nobler nervous elements are damaged 
secondarily. 

It is doubtful whether a simple, primary degeneration in the true 
nervous elements ever sets up inflammation secondarily in the vascu- 
lar structures. I know that in locomotor ataxia, a true degenerative 
disease, and in some degenerative forms of polyneuritis inflammation 



2,6 GENERAL CONSIDERATIONS UPON NERVOUS DISEASES 

of the meninges and of the interstitial tissues is often respectively ob- 
served but it is a question whether this inflammation is not due pri- 
marily to the same general infection or intoxication that gives rise to 
the degeneration. 

Degeneration as it is seen in the nervous system is a unique pro- 
cess. It gives a very characteristic appearance to the affected tissues, 
and its presence and progress render the symptomatology of nervous 
lesions clinically almost pathognomonic. Hence its appreciation is 
most important. As the distinctive lesion of the nervous apparatus, it 
is more important than the grosser lesions of vascular origin. When 
a nervous element undergoes degeneration it dies, wastes and dis- 
appears. The cell-body swells up, then becomes granular and fatty, 
and finally is absorbed. The process is sometimes called chromatolysis. 
In the early stage and temporarily, if the degeneration is not severe 
or complete, there may be a shriveling up of the cell-body; its edges 
then become serrated, its nucleolus disappears, its nucleus shifts to one 
side (decentralization), the chromophyllic particles diminish in amount 
and closely hug the nucleus while open spaces appear in the substance 
of the cell-body (vacuolation). Such cells sometimes regenerate, pass- 
ing through a reverse order of events. 

In acute and complete degeneration the neuraxones participate in 
the cellular destruction. The white substance of Schwann breaks up 
into fatty globules, the nuclei of the neurilemma proliferate, and the 
entire process becomes a hollow tube containing the axis-cylinder and 
degenerated white substance. At length the axis-cylinder breaks down ; 
absorption takes place, and nothing is left. Into the hollow space 
vacated by the process, or neuraxone, the neuroglia and connective- 
elements crowd and thus render the tissue firmer and denser, more 
vascular and less puctuated from nerve fibres on cross-section (scler- 
osis) than it was before. 

Degeneration may be an acute or chronic process, severe or mild, 
partial or complete. Most important is the fact that it may be primary 
or secondary. Under certain circumstances it may involve the entire 
neurone or only a part of it. It may spread directly from one neurone 
to the next one in the same nervous pathway, provided the second neu- 
rone is functionally subordinate to the first. This explains the morbid 
anatomy of the progressive system diseases. It probably never passes 
directly from one neurone laterally across to another lying beside it. 
The simultaneous degeneration of the two neurones under such circum- 
stances is in all probability due to the simultaneous action of the same 
cause. 

The origin of these degenerations lets a flood of light in upon the 
etiology of nervous diseases. The primary degenerations may be due 
to hereditary, congenital, toxsemic, nutritional and traumatic influ- 
ences. When the vitality of the neurones, transmitted from the parent 
to the child, is so vitiated that they cannot develop properly, function- 
ate normally, or resist the deleterious influences of life, they are neuro- 
pathic and break down into the condition of disease. In this way the 
developmental and familial diseases are eyolved. Friedreich's ataxia 
and the progressive atrophies furnish capital illustrations. In all prob- 



GENERAL CONSIDERATIONS UPON NERVOUS DISEASES 



0/ 



ability, it is only degree that distinguishes the neuroses such as epilepsy, 
migraine, congenital neurasthenia and hysteria from the cited ex- 
amples. 

Congenital primary degenerations are undoubtedly due sometimes 
to shock and malnutrition of the mother and then of the child while 
the latter is in the uterus. One must not confuse with these cases 
the infantile hemiplegias in whom secondary degenerations occur as 
the result of hemorrhage, inflammation and other factors. The con- 
genital primary degenerations are non-hereditary for they are intra- 
uterine in origin. Most of them, like most of the natal, postnatal and 
adult primary degenerations, are due to general or local traumatic, nu- 
tritiona.1 and toxsemic influences. 

Profound shocks, blows and concussions, without causing any 
discoverable lesion, are not unfrequently seen to provoke degenerative 
troubles, particularly of the mild type of the neuroses. Some of these 
even go on to severe degenerative alterations pronounced enough to 
be manifested in permanent paralysis. 

Malnutrition as a cause of degenerative trouble needs but to be 
mentioned. Local malnutrition occurs from vascular obstruction by 
emboli, thrombi and arteritis obliterans. Many senile forms of nerv- 
ous degeneration are due to inefficient nutrition and metabolism. 

The supreme cause of the primary degenerations in adult life 
are the intoxications and infections. I might have said only the intox- 
ications, for in the infections it is the poisonous products of the germs 
and not the germs themselves that provoke the degenerative changes. 
Under the head of etiology in the previous chapter I have referred 
to the various kinds of intoxication. Just how these intoxications 
act upon the nervous elements is not clear. Some probably damage 
them directly ; others doubtless affect them indirectly by lowering the 
nutritive value of the blood. Much has yet to be learned upon this 
question. 

Perhaps the greater number of nervous degenerations are sec- 
ondary in origin. The function of self-nutrition for the entire nervous 
element seems to reside in the cell body. Therefore if the cell body is 
damaged, all parts of the neurone undergo a parallel wasting. If a 
part of the neurone, say a part of the neuraxone, is severed from its 
cell-body, all that part that has been cut off wastes away. 

The latter is the well-known Wallerian type of denegeration. 

Now the factors that may damage the cell-bodies of a mass of 
neurones, or lacerate and sever their processes from them, are innu- 
merable and as a rule belong to the diseases and lesions of the con- 
nective tissue, the vascular and sustentacular elements generally. It 
is not necessary to describe these in detail but it is important to note 
that the localization of the lesion is rendered ofttimes very definite by 
the limited and definite area of destruction. As these lesions impli- 
cate more or less transversely the nervous paths, the degeneration 
travels in opposite directions away from it. Remaining always in the 
same system wherein it started, it advances upwards in the sensory 
and downwards in the motor paths if the lesion is anywhere between 
the cerebral cortex and the posterior spinal ganglia. If the lesion be 



38 GENERAL CONSIDERATIONS UPON NERVOUS DISEASES 

outside of the posterior spinal ganglia and include the paths of both 
the anterior and posterior roots, the degeneration will be downward 
in both the motor and sensory fibers in the nerves beyond the seat of 
the lesion. There will be no degeneration on the proximal side of the 
lesion. 

Secondary degenerations being due to damage of the neurone 
bodies or severance of the neuraxones from their nutritive centers, they 
are confined more distinctly and prominently to the neurones imme- 
diately involved. The next adjoining lower or higher neurones are 
but slightly affected and then only when they are functionally subor- 
dinate and dependent. 

In this respect there is a difference between the primary degener- 
ations due to such general influences as heredity and intoxication, and 
the secondary due to separation of a neurone or part of it from its 
nutritive center. 

Though localization symptoms may appear with the primary de- 
generations and in some particular cases be well-defined, they will be 
most pronounced and therefore most valuable in the secondary degen- 
erations. The whole question of localizations will be discussed however 
elsewhere. 

The constant characteristic of all those lesions, whatever their 
original cause may have been, that eventuate in secondary degenera- 
tion is that they involve vascular tissues and sooner or later are ac- 
companied by inflammation. Perhaps the only exception to this rule, 
and that is more apparent than real, is the case wherein a local area 
of nerve substance undergoes softening from the shutting off of its 
blood supply by an embolus or a thrombus. In this case the degenera- 
tion is of the primary type, though the lesion is grossly local and vas- 
cular. In all other cases, vascular trouble enters into the lesion with 
the appearance of more or less inflammation and secondary degenera- 
tion. 

Inflammation, therefore, is a most important feature in the pathol- 
ogy of the nervous system. The inflammatory process itself is iden- 
tically the same as it is elsewhere in the body. There is the same ini- 
tial hyperemia, extravasation of red corpuscles, infiltration of leu- 
cocytes, redness, swelling, softening and oedema. All this of course 
damages the delicate neurones lying in the midst of it. They undergo 
the degenerative process which usually terminates in complete func- 
tional and structural annihilation. 

The number of neurones that may be implicated is always a varia- 
ble one, depending upon the virulence of the cause and the violence 
of the lesion. Many neurones weather the storm and regain their func- 
tional integrity after the inflammation subsides. 

As inflammation is the reaction of the organism to an irritant, 
whether traumatic or infective, it is really a reparative process, an effort 
of nature to rid herself of noxious conditions. It is therefore always 
regressive rather than progressive and tends to limit itself so soon as 
it conquers the baleful cause which brought it into existence. In the 
warfare which it is carrying on against the agents of harm, it causes 
damage itself, some of which remains as a sort of a scar long after- 



GENERAL CONSIDERATIONS UPON NERVOUS DISEASES 39 

wards in the conditions of sclerosis, cavity-formation and atrophy. 
Among the last of course are to be included the secondary degenera- 
tions. 

Usually we recognize three types of inflammation in the nervous 
system, just as we do elsewhere. They are the simple exudative, the 
purulent and the so-called productive or proliferative inflammation. 
The former two are acute or subacute processes and differ from each 
other in regard to the presence of pus. The last is a chronic process ; 
is characterized by little congestion and exudation but rather by the 
slow formation of connective tissue. 

The cause of all these inflammations is not the same of course, 
some being due to mechanical, others to chemical, and still others to 
bacterial factors. 

It is unnecessary to discuss these further here as they are not at 
all peculiar. 

Among the residua and after-effects of inflammation in the nerv- 
ous system there are several of great importance. The secondary de- 
generations I have already spoken of. There is often local softening, 
general destruction and necrobiosis in the vicinity, with a mass of de- 
bris consisting of broken down nervous tissue, and blood elements. 
This undergoes absorption and leaves a scar or cyst in some cases. In 
others, especially when the inflammatory process has been chronic, 
sclerosis takes place. By this term is meant a hardening of the tissues 
from an overgrowth of the connective tissue elements and the replac- 
ing of the wasted true nerve cells and processes by them. The neu- 
roglia usually proliferates also. 

In sclerosis then we observe an absence or diminution of the num- 
ber of neurones with an increase of the neuroglia and connective tis- 
sue. Whether the overgrowth of the sustentacular tissue is first, caus- 
ing destruction of the neurones by compression, or whether the neu- 
rones degenerate first and the sustentacular elements proliferate to fill 
up the vacuity, is net always easy to determine. It is generally con- 
sidered, however, that the latter method occurs in the primary degen- 
erative diseases, whereas the former mode obtains in the inflammatory 
and secondary degenerations. 

From what has been said under the head of degeneration, it is 
easy to infer that when the neurone-cells are destroyed they are never 
regenerated. 

This is a fact of common observation and accounts for the perma- 
nency of many forms of paralysis and trophic disturbance. A neu- 
raxone that is destroyed may, however, completely regenerate. Just 
how it does so is not minutely known. All evidence seems to point 
out that the neurilemma and white substance of Schwann grow again 
in situ, but that the axis-cylinder extends forward from the proximal 
or cellular end into the new nervous tissue. The former reappear some- 
how from the local elements, whereas the latter steadily pushes for- 
ward like a branch growing from the trunk of a tree. It grows of 
course always from the trophic center. 

So'me recent experiments made at the University of Chicago 
demonstrate in the lower animals that neuraxones can thus extend 



40 GENERAL CONSIDERATIONS UPON NERVOUS DISEASES 

across lacerations and other forms of solution of continuity in the cen- 
tral nervous system. 

An interesting pathological condition which belongs solely to the 
nervous system is what is known as gliosis or gliomatosis. It is the 
basis of a certain form of tumor and cavity formation. It is essen- 
tially a proliferation of the glia cells and neuroglia tissue. Being non- 
vascular and epiblastic in origin it undergoes both primary and sec- 
ondary degeneration. In certain states of embryonic defectiveness, it 
proliferates, breaks down, is reabsorbed and leaves a cavity. Syringo- 
myelia is such a case in point. Sometimes with or without apparent 
cause, it spreads out and creates a tumor-like formation. These are 
the well-known gliomata of the nervous system. Finally it joins in the 
proliferative process of the connective-tissue elements in the production 
of the scleroses of the. cerebrospinal axis. 

In regard to the diseases of the nervous system in which no patho- 
logical changes can be discovered we can only argue, form hypotheses, 
and balance our logic. It is a time-honored custom to call such diseases 
functional, and to describe them as depending upon change of func- 
tion without change of structure. I must confess that I am incapable 
of comprehending such a paradoxical condition. I cannot grasp the 
idea that an abnormal manifestation can be the outgrowth of a normal 
structure. It is argued, however, that malnutrition, and possibly 
slight blood changes, are the cause of the functional disturbances. 
When pushed to the wall, those who argue thus say that they presume 
there may be some temporary physical or physio-chemical change in 
the neurones as a result of the malnutrition or reflex irritation. That, 
however, is included in what I conceive of as change of structure. It 
is too fine for our present means of detection undoubtedly but logic 
can penetrate often where physical means of research fail utterly. Logic 
seems to me to affirm beyond all question that an attribute of a thing 
cannot alter in the slightest degree without some alteration in the 
the thing itself. An attribute does not exist apart from the thing. It 
is but another point of view from which we behold that thing. A func- 
tion is an attribute of a functionating body. It has no more real ex- 
istence apart from that body than has its color, consistency or shape. 
Not one of the latter can vary without some variation having taken 
place in the body. In the same way, the function cannot change, it 
seems to me, without a change having taken place in the functionating 
substance. Of course this has no reference to what may be called sec- 
ondary functions or functions resulting from the action of one normal 
structure upon another. Psychosis is a secondary function, for it is the 
result of the interplay of certain elementary impulses. An abnormal 
psychosis may be a functional trouble with a normal physical basis. 
This is further discussed under hysteria. 

Therefore, in my opinion, there is a pathology for the so-called 
neuroses and functional diseases. ( )ur knowledge of it, like our knowl- 
edge of a good many other things, is still wanting. In their last 
analysis, functional diseases are as organic as any degenerative disease 
but not to so great a degree or so grossly as in what are commonly 
denominated flic organic diseases. 



GENERAL CONSIDERATIONS UPON NERVOUS DISEASES 41 

As a resume of the pathology of diseases of the nervous system 
the following schema may be useful : 

A. Pathological changes distinctively and primarily Neural (in- 
cluding the Neurones and the Neuroglia). 

a. Malformations ; Hereditary and Congenital Defects; In- 
complete Development or Agenesis ; Defective Development 
or Dysgenesis. 

b. Degeneration, Primary and Secondary. 

c. Gliosis and Gliomatosis. 

B. Pathological changes, not distinctively nor primarily Neural 
(including the connective tissues, blood-vessels, lvmphatics and epithe- 
lia). 

a. Inflammations. 

b. Hyperemia, Anaemia, Hemorrhage, CEdema, Arterial and 
Venous Diseases generally. 

c. Connective Tissue Sclerosis. 

d. Infective Processes like Tuberculosis, Syphilis, etc. 

e. All Neoplasms, Tumors, Parasitic Growths, Cysts, Ab- 
scesses, etc. (excepting Gliomata). 

GENERAL CONSIDERATIONS UPON THE SYMPTOMAT- 
OLOGY AND DIAGNOSIS OF DISEASES OF THE 
NERVOUS SYSTEM AND THE EXAMINA- 
TION OF THE PATIENT. 

It will be most appropriate to discuss the general semeiology of 
diseases of the brain, spinal cord, nerves and sympathetic system at 
the head of the sections devoted to these diseases and immediately after 
the consideration of the anatomy and physiology of the respective, parts 
of the nervous system. In this chapter I will take up, merely in a gen- 
eral way, the symptoms that belong to the nervous system as a whole, 
and will attempt some practical suggestions in regard to the proper 
method of examining a patient. 

On account of the inaccessibility of the nervous apparatus to direct 
examination, except in the one little spot back of the eye, 
and on account of the multiplicity and interrelations of its 
functional activities, the examination of it is a supreme test of the 
physician's natural ingenuity, skill and knowledge. One must ap- 
proach it with his mind completely unbiased, alert, and flexible. New 
points of view must be taken when unexpected hints are thrown out 
by the patient or his guardians. No opinions must be formed until the 
examination is finished, and even then it is sometimes well to with- 
hold them until after two or three future examinations. Snap diagno- 
ses are especially dangerous in neurology. There are geniuses, ex- 
ceedingly rare and far between, however, who can instinctively grasp 
the full situation after the patient has uttered a few sentences and ex- 
hibited a few signs. Even they sometimes make outrageous blunders. 
The more experienced a man is and the more learned in regard to the 



42 GENERAL CONSIDERATIONS UPON NERVOUS DISEASES 

nervous mechanism of course the more swiftly and accurately will he 
arrive at his final diagnosis. It is the safest plan for every one, how- 
ever, to be patient and painstaking, to omit no details and to weigh and 
test every phenomenon even to the point of tediousness. 

A mere glance at the anatomy and physiology of the nervous sys- 
tem demonstrates how absolutely necessary that every organ, tissue and 
function must be closely interrogated. In this respect a neurological 
examination differs pre-eminently from every other that the medical 
man is called upon to make. Only in cases of the greatest emergency 
should a hurried manner and a quick diagnosis be adopted. It is un- 
fortunate, though necessary of course, that such has to be done even 
then, for it is sometimes the cause of some very sad mistakes. When 
there is grave doubt, or not a reasonably clear symptomatology under 
these circumstances, the physician will do well to do nothing. Under 
such conditions nature is less liable to err than is human blindness. 

When there is no emergency or need of special haste, the phy- 
sician should first note carefully all of the attendant circumstances sur- 
rounding the patient. If he visits the latter at his home he should ob- 
serve the environment as closely as possible, for hints are sometimes 
thrown out in this way in regard to the mental and social status, the 
mode of life, the joys and the sorrows. The relatives and companions 
about him may be highly suggestive. Alcoholic coma might not in- 
appropriately be thought of in a saloon ; hystero-neurasthenia in a girl 
might justly be suspected if a brutal father and a termagant mother 
are present ; trouble from excessive mental study would hardly be ex- 
pected where there were no signs of a book. 

The patient's own attitude must be quickly remarked and the 
changes it undergoes during the examination. By the attitude I mean 
both the physical and the mental. 

It is wise to examine the patient alone and in the presence of oth- 
ers. In hysteria it is sometimes risky to remain alone in the room 
with the patient, but the door can be left partly open while the friends 
and relatives are in a distant room. The presence of one of the latter 
when distasteful may cause all sorts of irregularities in the symptoms. 
A temporary change of environment often astonishingly changes the 
complexion of things. I remember a woman who was sent to a pri- 
vate hospital several times by me. It was almost ludicrous how reg- 
ularly as clock-work she flew into her hysterical attacks at home while 
during weeks at the hospital she was as docile and reasonable as any 
creature. Syphilitics will often admit to the consultant, who charges 
them a good fee and for whom they have therefore perhaps an exag- 
gerated reverence, the disease that they have constantly and strenu- 
ously denied to their family doctor. 

Get the patient always, if possible, under other conditions and 
examine further before forming a final opinion. 

Avoid leading questions in eliciting the history of the case. Neu- 
rotics are particularly open to suggestion. I have seen diagnoses made 
that were really constructed on the semeiology suggested by the doc- 
tor and acquiesced in by the susceptible patient. This is an easy and 
common pitfall and should be carefully guarded against 



GENERAL CONSIDERATIONS UPON NERVOUS DISEASES 43 

Let the patient first tell his own story, often in his own verbose 
way, for thereby most valuable hints may be dropped and leading lines 
of examination suggested. After he has said all he has to say, then 
let the relatives and associates tell their story. Even let them give 
their opinions. Be most patient with them for they are reasoning, 
albeit ignorant laymen ; and the very picturesqueness of their descrip- 
tion, the energy and interest with which they tell of the patient's 
strange exhibitions, the biased yet unbiased attitude of mind in which 
they are, may go a long way toward giving a complete clinical pic- 
ture, whereas a too close limitation to the mere scientific data may lead 
to some confusion. 

In the examination of hysterics, epileptics and the insane we have 
to depend very largely upon the accounts of the family and of the 
friends. We must, however, be always guarded against letting their 
views determine ours. A nice adjustment between the medical and 
the lay prejudices will here reveal the keen examiner and the skillful 
physician. 

During the telling of the history of the case by the relatives note 
the trend of their ideas and the degree of their intelligence. The pa- 
tient may have moved intellectually beyond their sphere, and his en- 
vironment being uncongenial he may act in a way that seems queer to 
them but is not entirely illogical. This is the origin, in a large meas- 
ure, of the popular conception of the insanity and eccentricity of 
geniuses and of artists. 

After acquiring all the information he can from the patient and 
"his friends, the physician takes up the examination himself and while 
allowing them to interject an occasional remark that may add new light 
to some things, he avoids being diverted from his own course of proce- 
dure. He should have a general systematic method whereby to con- 
duct his examination, else he will be certain to overlook many things. 
Even though he may not have to go through the whole form even- 
time before arriving at a diagnosis, it is nevertheless good to do so 
because important matters may thus be brought out, time may really 
"be saved in the end, and the practice of being systematic may develop 
a desirable facility for examining future patients. A scheme some- 
what like the following may be adopted, even printed out in one's 
case book : 



44 



GENERAL CONSIDERATIONS UPON NERVOUS DISEASES 



Name Age Sex Nationality Occupation . 

Marriage Temperament Culture Date. . . 



Family History: 

Grandparents 

Parents 

Brothers and Sisters 

Other near Relatives 

Personal History : 

Habits as to Diet 

Habits as to Alcohol 

Habits as to Tobacco and Drugs . 

Habits as to Venery 

Inherited and Acquired Dis- 
eases : 

Syphilis 

Gonorrhoea . . 

Other Infections 

Condition of the — 

Lungs 

Heart 

Arteries 

Alimentary Tract 

Genito-Urinarv Tract 



Traumata 

Deformities 

Pulse 

Temperature 

Respiration 

Urine 

Gait 

Attitude 

Patient's Account 
Trouble in Brief 



of Pre? em 



Motor Symptoms . 
Sensory Symptoms 



Reflexes 



Electrical Phenomena 



Vasomotor and Secretory Symp- 
toms 



Trophic Symptoms 
Eye and Vision . . . 
Ear and Hearing. . 
Nose and Smell. . . 
Mouth and Taste. . 
General Remarks . 



Voice 

Speech 

Handwriting Diagnosis 

Psychic Symptoms 

The diagnosis of disease of the nervous system depends upon both 
etiology and symptomatology. It must be made from aJl available phys- 
ical and mental data. Its end is the determination of the actual exist- 
ence of a nervous disease, the character of the lesion and its loca- 
tion. 

The real presence of a nervous disease is decided almost wholly by 
etiological factors and a few observable changes like a choked disc or 



GENERAL CONSIDERATIONS UPON NERVOUS DISEASES 45 

muscular atrophy. In other words not all motor and sensory and 
psychic' abnormal manifestations represent actual disease. Simulation 
and malingering may be present. Suggestibility may provoke mislead- 
ing exhibitions. Secondary irritation from extraneous conditions of 
all sorts, both in and out of the body, may give rise to the exaltation 
or suppression cf nervous functions that closely imitate inherent nerve 
trouble. 

It is sometimes the hardest part of the diagnosis to determine 
whether there is an actual disease of the nervous system present. No 
fast rules can be laid down for determining this. It is all a matter 
of the logical ability, the shrew T dness, the skill, and the knowledge of 
the diagnostician. 

When it is recognized that an actual disease of the nervous sys- 
tem is present, the nature of it must be decided by a careful study of 
both its etiology and symptomatology. The location of the lesion is 
inferred almost wholly from the symptoms, though the etiology helps 
in determining it slightly in some cases. 

In the preceding chapter upon pathology, I have pointed out some 
general facts in regard to the nature of the various lesions and how 
they may be inferred. Localization symptoms will be taken up at the 
head of the various sections devoted to the brain, the spinal cord and 
the nerves. 

The gait of the patient in walking is a most obvious symptom 
sometimes, and to one experienced in nervous troubles will alone often 
suggest the diagnosis. The hemiplegic, the tabetic, the victim of dis- 
turbed equilibrium of the cerebellar or other type, and of spastic para- 
plegia, can almost instantaneously be recognized. 

The attitude, with or without the peculiar gait, is frequently very 
significant. Who does not recognize the characteristic stoop and posi- 
tion of the hands in paralysis agitans? Even the laity notice the list- 
less, fixed, indifferent position of the victim of melancholia. If atti- 
tude were given more consideration, hysteria, neurasthenia, many forms 
of psychosis and not a few organic troubles would almost be suspected 
at once sometimes. The attitudes of disease are not infrequently path- 
ognomonic. 

While the patient is giving his account of the first appearance of his 
present trouble and of its course and symptoms up to the present mo- 
ment, note carefully the character of his voice and the mode of his 
speech. Does he speak loudly or softly? Is his voice rasping or 
smooth? Is there aphonia and does he have to whisper? Observe 
whether he trips in his speech or runs his words together or scans 
his sentences as if he were scanning a line of poetry. Does he omit 
or repeat words or introduce irrelevant words into his sentences? Ask 
him to read and note if he does the same thing when reading. Aphonia, 
dysarthria and aphasia will all be discussed after the consideration of 
the physiology of the brain. They are mentioned here simply to im- 
press the importance of noting them carefully in the course of the ex- 
amination. Agraphia, trembling and other impediments to writing will 
also be described elsewhere. 

Psychic symptoms are hardly of less importance in neurology than 



46 GENERAL CONSIDERATIONS UPON NERVOUS DISEASES 

they are in psychiatry. The mind is the product of cerebral activity, 
and cerebral activity is provoked by afferent nervous impulses. It 
may be interesting but hardly profitable to discuss such questions as 
the immateriality of mind and the duality of man's nature. We have 
no proof, that can be called scientific, of a consciousness apart from 
cerebral function. To say this is not to deny the mind's possible im- 
material existence ; it is merely affirming the scientific limitations of 
the question. 

To escape all such gross notions as mental telepathy, mental trans- 
ference, mind-reading, clairvoyance, spiritism, etc., one has but to 
recollect that psychic phenomena are never known to occur without 
simultaneous cerebral phenomena. Dead brains have never, in all 
the ages, given the slightest evidence of the presence of mind, and 
mind has never been observed apart from living brains. 

This interdependence is further shown in the parallelism that ob- 
tains between physical disease and mental aberration. In many cases 
actual gross changes are observed in the brain ; in others the changes 
are so slight that our present means of investigation cannot detect 
them. It is not improbable that a disturbance of the normal flow of 
inpouring sensations, by means of various nervous and other diseases, 
may underlie a large number of the phenomena of psychiatry. At 
all events, as the nervous system is the seat of the mind pre-eminently, 
and as it is the apparatus upon which it seems immediately to depend 
both for its own portrayal, activity, and communication with the outer 
world, it is obvious that mental symptoms are of immense significance 
in neurology. 

A detailed description of these symptoms will be more appropri- 
ately considered along with the physiology of the brain. It may be 
noted here, however, that chief among them are the mental stigmata 
of degeneracy, abnormal emotional states with exaltation or depres- 
sion, delirium, maniacal violence, illusions, hallucinations and delusions, 
loss of consciousness, or coma, double consciousness, amnesia, aphasia, 
word-deafness, word-blindness, agraphia, etc. 

Motor and sensory symptoms have very dissimilar diagnostic valu- 
ation. The motor symptoms, being objective and capable of being ex- 
amined apart from the patient's consciousness, are the more definite, 
distinct and reliable to base a diagnosis upon. 

The sensory symptoms are almost wholly subjective. To be sure 
we can infer a good deal objectively in reference to them by varying 
ourselves the stimuli that provoke them and by testing them in the 
reflex arcs; but nevertheless even here it is practically impossible f o 
eliminate entirely the patient's consciousness during their examine 
tion. Under ether narcosis they are not in evidence even in relation 
to the reflex arcs. 

Too much stress, therefore, should not be laid upon sensory phe- 
nomena except in association with others. They are. however, the 
most important symptoms to the patient and sometimes the only ones. 
Their greatest value, after their reality has been positively determined, 
is in the localization of the lesion. The psychic nature of hysteria is 
all but positively affirmed by the peculiar distribution and prominence 



GENERAL CONSIDERATIONS UPON NERVOUS DISEASES 47 

of its sensory symptoms. A moving myelitis can sometimes be beau- 
tifully watched by the rise and fall of the border-line of anaesthesia. 

The symptomatic significance of the various forms of sensory dis- 
turbance will be referred to again in the introductory chapters to the 
special diseases. Only some general features will be noted here. 

There are five forms of sensation, commonly spoken of as gen- 
eral and special sense. Biologically they are all evoluted out of com- 
mon or simple touch sense. So far as the nervous apparatus itself 
goes there are nothing but afferent impulses. The naming of these 
impulses, touch, pain, heat and cold, sight, smell, taste and hearing, is 
the result of the special end-organs in connection with the nerves. A 
nervous atrophy that produces blindness, for instance, is no different 
from a nervous atrophy that produces cutaneous anaesthesia ; the form 
of nervous lesion that causes auditory hallucinations may be exactly 
the same as the form of nervous lesion that causes a paresthesia. 

With all the sensory phenomena, therefore, there should be a most 
careful determination as to whether the lesion resides in the outer end- 
organs, the receiving brain centers, or the intervening nervous pathway. 
It would be ludicrous, if it were not so tragical, to note how frantic- 
ally and persistently glasses are worn and changed, even upon the 
recommendation of careless and ignorant opticians, for a fading eye- 
sight, when an examination of the eye-ground would reveal a progres- 
sing optic atrophy. 

It is a common fact for the pains of tabes, a central disease, to 
be mistaken for the pains of rheumatism, a peripheral trouble. 

The diagnosing of the presence of a sensory disturbance is not 
enough. It must be determined why and wherefore the disturbance is 
present. 

In the skin are located three forms of common sensation, namely, 
touch, pain and temperature sense. 

In the muscles, tendons, fascia, joints and contiguous structures 
there is what is called a muscular sense, a sense which gives us some- 
what an idea of the location of the limbs. 

The nature of the latter sense is not clearly established yet and 
some authorities even doubt its existence as a special sense. 

The cutaneous and muscular senses are as much dependent upon 
special end-organs for their differentiation as are the so-called special 
senses of hearing, smell, taste and sight. 

When a sensation is excessively or abnormally acute we speak 
of the condition as hyperesthesia. When it is abnormally dull we re- 
fer to it as hypcesthesia. If it is absent entirely it is anesthesia. Per- 
verted sensations such as numbness, "pins-and-needles" feeling, formi- 
cation or the sensation as of ants crawling over the skin, are known as 
paresthesia. 

These terms have been so universally applied to the tactile sense 
alone that, I am satisfied, it has had a good deal to do with keeping 
alive the common notion that special sense is in some way something 
extraordinarily different from the sense of touch. Nerve blindness is 
nothing but optic anaesthesia ; visual hallucinations, like flashes of light, 
fortification figures, are really, when of nervous origin, only instances 



48 GENERAL CONSIDERATIONS UPON NERVOUS DISEASES 

of optic paresthesia. This should never be forgotten as it will save 
one from propounding such absurd questions as, Why should blind- 
ness occur in hysteria along with cutaneous anaesthesia, as a notable 
symptom? A proper knowledge of the basic character of all sensa- 
tion would cause the question to be asked, Why shouldn't it occur? 

Disease, it must be remembered, may attack the end-organs and 
produce hyperesthesia, anesthesia or paresthesia; a cataract produces 
blindness ; a scar in the skin causes local loss of sensation ; the loca- 
tion and lesion are unlike but the manfestations are the same, anes- 
thesia, but not pure neural anesthesia. Atrophy of the optic nerve and 
atrophy of the spinal sensory nerves cause respectively loss of vision 
and loss of the sense of touch ; the lesion is the same but the location 
merely is different. That is pure neural anesthesia. Destruction of 
the visual centers in the occipital cortex and destruction of the sen- 
sory centers in the parietal cortex alike cause sensory anesthesia. 

The universality of irritability in the nervous system is a most im- 
portant fact for it helps to give valuation to these phenomena as a 
means of localization, since it is thus varied merely by reason of the 
connections which the nervous apparatus makes. In this respect the 
sensory apparatus is the same as the motor wherein we localize lesions 
chiefly by the particular muscles with which it is connected. 

For the alterations in the pain sense we use the terms hyperalgesia 
and analgesia. Sometimes pain arises spontaneously in an analgesic 
area. This is known as analgesia dolorosa. 

Thermancesthesia is of course a loss of the temperature sense; hot 
and cold are not felt at all, only the touch of the heated or frozen ob- 
ject. In syringomyelia this is a remarkable and troublesome symptom. 

A localized pain without a known cause is a topoalgia. 

Causal gia is a pain like that of burning. 

Polycesthesia refers to successive repetitions of a sensation after 
one stimulation. 

In macrocesthesia objects feel larger than they actually are. 

A sensation may be quite normal in all respects except in being 
delayed. This is not an uncommon phenomenon and must always be 
looked for. 

Transference of a sensation is a curious exhibition sometimes 
called allochciria. A stimulation on one side of the body is referred 
to a similar spot on the other. 

Ataxia or incoordination of movement, astereognosis or loss of the 
sense of the shape of objects when held in the hand, and loss of reflex, 
are some of the sequele of disturbed sensation that will be discussed 
more in detail elsewhere. 

A knowledge of the sensory innervation of the skin is necessary 
for localization purposes. 

To test the sensations demands but a little ingenuity. Touch can 
be examined by passing lightly over the skin, with the patient blind- 
folded, a camel's hair brush, a piece of raw*cotton or other light, soft 
object. Note the quickness of the response, the accuracy of the local- 
ization and how it feels to the patient. 



GENERAL CONSIDERATIONS UPON NERVOUS DISEASES 49 

The temperature sense is proved by the application to the skin 
of a piece of ice or a test-tube filled with hot water. 

The use of excessive heat, pricking with a pin, or pinching will 
tell whether the pain sense is lost or not. 

The muscular sense is noted by placing the limbs in different 
positions, while the patient is lying in bed, and asking where they 
are without his looking at them. Place various weights in his hands 
and note whether he remarks the difference. This tests the pressure 
sense. Any small object like a watch, a key, a match-box, placed in 
the hand will aid in the detection of astereognosis. The patient gives 
an erroneous description of its shape or says he cannot describe it at all. 
• The costhesiometer is a compass-like apparatus with a graduated 
scale on it for the accurate measurement of the tactile discrimination 
in the skin. The two points of a hairpin or pair of sharp scissors may 
even be conveniently employed. The tongue, tips of the fingers and 
lips are the most sensitive parts of the body and serve well for tests 
with the sesthesiometer. In order to have a normal standard ready 
at hand for purposes of comparison, the following table from Weber, 
indicating the shortest distances and the parts of the body on which two 
points can be recognized, is presented. 

Tip of tongue 1-24 inch. 1 Aim. 

Palmar surface of third phalanx of forefinger. . . 1-24 inch. 1 Mm. 

Palmar surface of second phalanges of fingers. . 1-12 inch. 2 Mm. 

Red surface of underlip 1-6 inch. 4 Mm. 

Tip of nose 1-6 inch. 4 Mm. 

Middle of dorsum of tongue 1-4 inch. 6 Mm. 

Palm of hand 1-3 inch. 8 Mm. 

Center of hard palate 5-12 inch. 10 Mm. 

Dorsal surface of first phalanges of fingers 1-2 inch. 12 Mm. 

Back of hand 7-12 inch. 14 Mm. 

Dorsum of foot, near toes 1 1-6 inch. 25 Mm. 

Gluteal region 1 1-2 inch. 37 Mm. 

Sacral region 1 1-2 inch. 37 Mm. 

Upper and lower parts of forearm 1 1-2 inch. 37 Mm. 

Back of neck near occiput 2 inch. 50 Mm. 

Upper dorsal and mid-lumbar regions 2 inch. 50 Mm. 

Middle part of forearm 2 1-2 inch. 62 Mm. 

Middle of thigh 21-2 inch. 62 Mm. 

Mid-cervical region 2 1-2 inch. 62 Mm. 

Mid-dorsal region 2 1-2 inch. 62 Mm. 

Such wide variations of judgment occur among normal individuals 
that not much reliance can be placed on the sesthesiometer findings un- 
less they are very gross and constant. In general it may be consid- 
ered abnormal if the points have to be separated double the above dis- 
tances before they are able to be distinguished apart. 

The pain sense may be approximately measured and the differences 
observed by the employment of different strengths of the faradic cur- 
rent. Of course here as in all tests for sensation the eves must be 
covered, normal parts of the body must be compared with abnormal, 



5C GENERAL CONSIDERATIONS UPON NERVOUS DISEASES 

repetitions of the test must be made at different times and false touches 
and deceptions must be practiced to note the amount or presence of sug- 
gestibility. It is well to outline an anaesthetic area sometimes with a 
blue pencil or iodine brush and note the changes from time to time. 
Blanks with printed outlines of the body upon them are useful for keep- 
ing a record of such data. 

The special senses have their own particular ways of being exam- 
ined which will be noted under the heads of the respective cranial 
nerves. 

Motor phenomena usually owe their initiation to some form of 
efferent nervous impulse. Nerves and muscles make up a very compact 
and closely united neuromuscular apparatus. The nervous tissue in- 
cites the movement, the muscle executes it. Only under exceptional 
circumstances do muscles contract from other than neural stimulation. 
Direct irritation by blows or other means may in some instances cause 
the muscular fibrillse to contract, and undoubtedly muscular paresis re- 
sults from inherent muscular disease*. Nevertheless it is so true that 
the vast majority of muscular contractions are due to nervous stimu- 
lation, that it may be generally affirmed that disturbance of the former 
is indicative of disease of the latter. The impulse that provokes a mus- 
cle into activity usually has its origin in a nerve cell or neurone-body. 
It is not probable that direct irritation to the neuraxones of the motor 
neurones awaken muscular phenomena. In the cases in which irritation 
of the peripheral nerves provokes spasms, the sensory neuraxones are 
in all likelihood irritated and in a reflex way the motor side of the arc is 
put into functional activity. Motor impulses therefore always start 
from the cell-bodies of the motor neurones. They may arise de novo 
there or they may be the result of stimulation by the related sensory 
neurones. 

In all forms of motor activity, therefore, normal or exalted, the 
cell-bodies of the related motor neurones, are more or less implicated. 
If the activity is diminished or annihilated the trouble may be anywhere 
in the motor neurones, their cell-bodies or their processes. Hence mus- 
cular over-activity has a much wider origin than has under-activity. 
This is an important distinction when it comes to a question of diag- 
nosis. ■ Spasms are due to far more numerous causes than are paralyses. 

Beyond the mere statement that stimulation is present, we can 
offer no explanation as to how nerve force passes over into muscular 
force, how excitement merely provokes contraction. Much more im- 
portant is it to know that all muscular movements of neural origin are 
due to impulses from two sets of neurones, the upper and the lower. 
An examination of the neuronic architecture of the nervous system re- 
veals the fact that the muscles are under the direct and immediate con- 
trol of the neurones whose cell-bodies are in the gray matter of the 
cord and its homologue the cranial nuclei, and that they are under the 
indirect or mediate control of the neurones whose cell-bodies are in the 
cerebral cortex. Individual muscles therefore are the executive agents 
of the lower neurones ; generalized movements, inhibition, and control 
of the lower neurones constitute the primary purpose of the activity of 
the Upper neurones. 



GENERAL CONSIDERATIONS UPON NERVOUS DISEASES 5T 

So far as we know, the essential nature of nerve activity, the ex- 
pression of neurility, is identically the same in both sets of neurones. 
They differ in function solely on account of their respective end rela- 
tionships. Thus, as will be described more in detail in other sections 
of this book, they lend themselves by reason of the difference of func- 
tion to focal diagnosis. Individual muscle disturbances will point to 
the location in the cord or cranial nuclei. 

The disturbance of bodily movements will indicate quite as sharply 
just where the trouble is located in the cerebral cortex or its subsidiary 
structures. 

The symptoms upon which this localization diagnosis is to be made 
will be discussed at the head of brain and cord diseases. 

The character of the motor disturbance is indicative of both the 
location and nature of the lesion. As the cerebral set of neurones ex- 
ercise normally an inhibitory control over the spinal, when they are 
diseased that control is relaxed and the resulting motor disturbance is 
rigid and spastic in character. Where the disease involves only or pri- 
marily the spinal neurones, the disturbance is flaccid and limp in char- 
acter. In either upper or lower neurone disease, the lesion may be only 
such as to irritate and cause overaction or irregular action in the mus- 
cles. The irritative influence usually has its origin entirely outside 
of the neurone, either from disease in the sensory apparatus or in 
gross forms of trouble in the mesobiastic tissues. Lesions that are de- 
structive of the motor neurones are therefore usually inherent lesions 
and directly abolish the function of the neurones. Lesions that are 
merely irritative are more generally extraneous, affect the motor neu- 
rones secondarily, and exaggerate or otherwise disarrange their func- 
tion. 

The common evidence of destructive lesions is therefore paralysis, 
of irritative lesions spasm and inco-ordination. 

It is extremely important that the term paralysis or akinesis should 
be limited to the abolition of muscular movements from neural lesions 
alone. 

As I have already intimated, immobility may be due to many other 
causes, as for example ankylosis, muscular disease, rheumatism, frac- 
tures and dislocations. 

Both the voluntary and involuntary sets of muscles may be par- 
alyzed. 

There are degrees of paralysis so that we speak of complete and 
incomplete paralysis. The term paresis is sometimes used for the lat- 
ter. Individual muscles may be paralyzed or physiological groups of 
muscles concerned in particular forms of movement. A flaccid paralysis, 
is one in which the part hangs dead, limp, immobile ; a spastic paraly- 
sis, one in which there is stiffness, rigidity and tension in the part. 

A paralysis may have its origin in the higher psychic centers even. 
This is commonly spoken of as pseudoparalysis. 

The distribution of the paralysis is indicated by the use of s/ich 
terms as monoplegia, hemiplegia, paraplegia and crossed paralysis. As 
these belong to localizing signs, they will be referred to again. 

In testing a paralysis the patient should relax himself as completely 



52 GENERAL CONSIDERATIONS UPON NERVOUS DISEASES 

as possible and should be examined in various positions, in and out of 
bed. The normal physiological movements should be well known and 
the diseased side should be carefully compared with the well. First 
let the patient show what he himself can or cannot do. If the paralysis 
is only partial, take hold of the part and note the force of resistance 
exerted by the patient. 

The dynamometer is a graduated oval spring which can be used, 
by pressing it, to measure the comparative power of resistance. Its use 
is limited, however. Remember that the left side is normally weaker 
than the right. Paralysis of individual muscles can be sometimes tested 
thus, though in most cases it has to be noted by the attitude of the parr 
and by the electrical tests and associated atrophy. 

Tests for paralysis should be made repeatedly and varied in everv 
possible way. It should be noted whether there is the slightest shade 

FIGURE i. 




Dynamometer. 

of associated movement in the paralyzed member when the well one is 
stretched out. 

A little ingenuity and a perfect familiarity with the normal func- 
tions of the muscles are all that is needed for testing paralysis. Various 
instruments have been devised but immediate examination without in- 
struments of any sort will give a careful, skillful and experienced ex- 
aminer more and better information than an}' form of mediate test. 

Spasm or hypcrkinesis is an exaggeration of motility. Its real na- 
ture is hidden somewhat in obscurity, though it is probably due to exag- 
gerated or incessant nerve stimulation. It is not necessarily due to 
disease in the motor neurones. In fact, it is usually the result of irri- 
tation of these neurones by disease outside of them. The latter may 
be of a vascular or connective-tissue type, of a toxsemic nature, or a le- 
sion involving the sensory neurones. Muscular spasm is very often a 
mere reflex phenomenon and so far as the nervous system is concerned 
may not be the expression of disease at all. 

We do not know that there is any essential difference between 
tonic and clonic spasms except that the stimulating impulses in the 
former are so short and rapid in succession that the muscle fibres have 
no chance to relax and the whole muscle remains in prolonged and 
constant contraction. In clonic spasms there is an alternation of con- 
traction and relaxation so gross as to be easily observed. 

A cramp is nothing but a painful spasm. 

A convulsion is a spasm that involves the entire musculature of the 



GENERAL CONSIDERATIONS UPON NERVOUS DISEASES 53 

body or parts of the body. Convulsions may be tonic or clonic, co-ordi- 
nate or inco-ordinate. Unconsciousness usually accompanies a con- 
vulsion. 

Choreiform movements are spasmodic jerkmgs, in certain groups 
of muscles, irregular, inco-ordinate and more or less violent and par- 
tially under the control of the will. 

What is called convulsive tic is a very localized form of choreiform 
spasm, possibly even in one muscle, but more generally in a group of 
muscles that perform a certain physiological act. 

Athetoid movements, athetosis, consist of slow, ceaseless, waxy- 
like flexion and extension of the hands and feet and their various parts. 

Other forms of muscular spasm are the excessive muscular tension 
and contracture seen in some diseases. These are more or less perma- 
nent or at least chronic conditions and are consequently accompanied 
by a certain degree of organic change. If either one should disappear 
during sleep or under etherization, it would show that it was merely a 
functional trouble, probably hysterical. 

A forced movement is a sort of convulsion in which a patient in- 
voluntarily turns and moves in various peculiar but not altogether un- 
natural ways. He may whirl about suddenly or start off in a particular 
direction. 

Associated movements are another sort of curious, spasmodic phe- 
nomena. A limb lying at rest involuntarily performs the same or simi- 
lar movement that is voluntarily performed in the other limb. Hemi- 
plegic limbs sometimes thus move in more or less imperfect unison with 
the movements in the sound limb. 

As with paralysis so in cases of hvperkinesis, the localization of 
the lesion can be partly inferred from the distribution of the phenom- 
ena. We speak therefore of monospasms, hemispasms and other types. 
The symptom is so obvious that it requires no special skill to distin- 
guish it. 

Tremor is a fine clonic spasm, rhythmical, constant, independent of 
the will and due to faulty innervation. There is an ataxic form of it 
revealed upon volitional movement. The parts affected are kept con- 
stantly oscillating, usually without pain or marked exhaustion. The 
oscillations vary from 3 to 12 per second. When they are from 3 to 5 
per second the tremor is coarse, when from 8 to 12 it is fine. Weak- 
ness is usually associated with it. The ataxic tremor is badly named 
intentional tremor. 

Fibrillary tremor is one in which the phenomenon seems to be lim- 
ited to particular fasciculi in bundles of muscular fibres. It is often- 
times so delicate that it can only be detected by resting the linger on the 
part affected and feeling it. 

Tremor is often increased by voluntary effort, as witness the tremor 
of dementia paralytica when the patient attempts to speak or write. 

Incoordination of movement, or dyskinesis is a most important neu- 
rological symptom. We have already seen that incoordination of move- 
ment may be due 10 sensory disturbance. Such is the cause of it in 
locomotor ataxia for instance. The various attitudes assumed by our 
bodies, the gait adopted in our walking, the physiological movements of 



54 GENERAL CONSIDERATIONS UPON NERVOUS DISEASES 

all sorts, are the result of the harmonious combined action of a number 
of muscles. There is normally a nice adjustment between antagonistic 
or opposing sets of muscles so that action and counteraction are never 
allowed to pass beyond the point necessary to accomplish a given move- 
ment. Flexion is always nicely opposed to extension, pronation to su- 
pination, dilatation to contraction. This is an unconscious adjustment, 
though it is obviously submissive to the will. We can overflex the arm 
but we cannot release the extensors from their entire control of the ac- 
tion at the same time. We can close the orbicularis oris but we cannot 
prevent the other facial muscles from taking part in the performance. 
In some of the sphincters the will is entirely inoperative, and yet the 
sphincter functionates under an opposing inhibition. Whenever this 
adjustment is broken, the movements become most indefinite, irregular, 
ludicrous and bizarre. The volition starts the muscles to contract, but 
what they will do not even the patient himself can imagine. Anarchy 
seems to rule among them and most surprising exhibitions are pre- 
sented. 

Such is incoordination or ataxia. It is from its very nature not a 
disease of one anatomical structure, though it is the product many 
times of a more or less anatomically limited lesion. 

We have said that movements are the results of activity in the cell 
bodies of the motor neurones and that this activity may arise de novo, 
or as the result of sensory stimulation. When sensation is disturbed, 
one important cause of muscular action is at fault and as a result that 
muscular action itself is confused. 

Again, for most of the automatic and involuntary movements, such 
as walking and the contractions of the uterus in parturition, there is 
somewhere in the central nervous system an arrangement of neurones 
for the adjustment of the various muscular activities that go to make 
up the completed movements. 

And finally in all voluntary movement the adjustment is uncon- 
sciously managed so that all muscles work harmoniously together, for 
the accomplishment of the particular end in view. 

Ataxia therefore may result from a disturbance of afferent im- 
pulses, from disease in the central coordinating apparatuses, or from 
the upsetting of normal mentalization. In all of this there may be no 
essential motor disturbances, no paralysis, no spasm, but merely sen- 
sory and reflex and mental trouble. The movements are bizarre because 
their sources of stimulation are in an abnormal state. There may, how- 
ever, be a purely motor incoordination. One set of opposing muscles 
may be functionally disturbed, whereby the normal balance of power 
between the two sets is broken. Indeed the different parts of the same 
muscle, and even different sets of fibrils, may be so affected that an 
intramuscular incoordination obtains. This doubtless is the underlying 
cause of many forms of coarse and fine tremor of irregular character. 

As I have intimated ataxia is the typical form of incoordination. It 
may be sensory or motor, usually sensory, in origin or due to trouble 
in the central organs that subserve the maintenance of coordination and 
equilibrium. In ataxia the disturbance of the certainty of purposive 



GENERAL CONSIDERATIONS UPON NERVOUS DISEASES 55 

movements is most obvious or with a little ingenuity can be easily 
elicited. 

Sensory ataxia is beautifully seen in tabes ; sensory and motor 
ataxia is probably observed in multiple neuritis and disseminated 
sclerosis. 

Cerebellar ataxia, in which the reeling gait of acute alcoholism is 
most accurately imitated, is due to trouble in the central coordinating 
apparatus. 

Vertigo is a form of central ataxia, so also is the confusion some- 
times observed in the psychoses of mild and severe degree wherein the 
ideas of movement are concerned. 

It requires a harmonious action between muscles to maintain an 
attitude as well as to perform a movement ; hence there is static as well 
as motor ataxia. All the senses help in the maintenance of equilibrium, 
therefore shutting off the visual sense by closing the eyes causes a 
static or motor ataxia to be increased. 

All one has to do to test for ataxia is to ask the patient to per- 
form some complicated movement — walk a chalk line on the floor, touch 
the end of his nose with his finger while his eyes are shut. 

Speech may be ataxic in character and it may be of motor or 
psychic origin. This will be referred to again in the section on the 
brain. 

A most important nervous manifestation is that of reflex action. 
In fact, reflex action, which means in its last analysis nothing more nor 
less than stimulation and return response, is the fundamental raison 
d'etre of the nervous system. To be cognizant of external irritants 
and to send back appropriate counter effects to the part or parts 
related to the source of irritation, is what nervous tissue was biologically 
evolved for. 

There is thus an ingo and an outgo as the fundamental fact in 
all primary nervous manifestations. Every move in life, even thought 
itself, is but a reflex or a modification of a reflex. 

Impulses in some low forms of animal life may travel in and out 
over the same pathways. In the higher forms the afferent are different 
from the efferent pathways. Between the two, at their central ap- 
proximation, there may be interjected special cells or neurones to 
modify the impulse in its round from afferent to efferent path. 

A reflex action therefore is seen to involve a more or less compli- 
cated arc consisting of afferent^ central, and efferent elements. The 
first originates in the skin or o'ther special end-organ of sense and 
terminates in some central gray matter. This gray matter contains the 
modifying intervening neurones and is usually under the inhibitory 
control, to a certain extent, of the higher or cortical neurones. The 
efferent pathway starts in the central gray matter, and terminates in 
the muscle, gland or secretory organ. An irritation in the skin there- 
fore sends an impulse inward and around the arc until it expends itself 
finally in muscular action or altered secretion. In its course this im- 
pulse, under certain circumstances, may be halted by a central im- 
pulse sent down from the brain or it may send an impulse itself up to 
the brain. 



56 GENERAL CONSIDERATIONS UPON NERVOUS DISEASES 

That is in brief the whole picture of a reflex action. 

It is clear that a lesion anywhere in the arc, in the afferent, the 
central or the efferent tract, may put an end to the reflex. Moreover, 
disease in the controlling inhibitory path reaching down from above 
will undoubtedly modify the activity of the reflex arc. If the inhibitory 
control is destroyed, the reflex will of course be released ; if it is in- 
creased the reflex may be completely throttled. According to the loca- 
tion of the center of the reflex arc, and according to the terminations 
of either end of it, will the localization manifestations be in connection 
with it. Therefore the detailed description of the individual reflexes 
will be postponed until the discussion of the special parts of the ner- 
vous system is taken up. 

It may be well to state here, however, that there are recognized 
in neurological symptomatology, four kinds of reflexes, the skin, or su- 
perficial, reflexes ; the tendonous, or deep, reflexes ; the idiopathic mus- 
cle reflexes, and the visceral reflexes. 

Reflexes may be absent, or they may be merely exaggerated or 
diminuished. 

Reflex phenomena occur wherever there is a neuro-muscular ap- 
paratus, hence these phenomena are observed in connection with the 
sympathetic as well as the cerebrospinal system; in the organs, and 
the vasomotor apparatus of the body. 

The superficial or skin reflexes are best elicited by a slight touch, 
a gentle pinch, a pin prick, a tickling or a momentary application of 
cold or heat to the skin. The value of these reflexes as localization 
symptoms is variable, as will be pointed out elsewhere. The more im- 
portant of them and the method of provoking them are as follows. 

About the head many are obvious and are seen in the winking and 
the twitching of the facial muscles, and in animals in the shaking of 
the ears to remove insects and irritating objects. The scratching of 
the skin of the face or chin causes the pupil to dilate. Irritating die skin 
over the back muscles, as for example over the erector spinas and scap- 
ular muscles, causes the latter to contract. The same is true of the 
muscles of the abdomen and thorax ; cutaneous irritation at the sides 
causes them to contract, especially the rectus abdominis. 

The cremasteric reflex consists of the drawing up of the testicle 
when the skin of the inner thigh of the same side is pinched and 
tickled. The scrotum alone is not affected. The palmar reflex is of 
very little importance, but in sleep some people move the fingers when 
the palm of the hand is touched. The plantar reflex is usually well 
marked and in fact enters into the Babinski sign. This observer noted 
that when the sole of the foot is stroked, there is a difference between 
the movement of the foot and of the toes. Normally when the plantar 
skin is slightly irritated, the foot is thrown into dorsal flexion and the 
toes into plantar flexion. That is the ordinary, long-recognized, fa- 
miliar plantar reflex. Babinski noticed thai in disease, when the sole 
is tickled, dorsal flexion of the foot lakes place, but the toes, especially 
the great toe, undergo dorsal reflexion also, or what is the same thing, 
extreme extension. This is a must important criterion oi disease. 
though its fullest significance we have yet to learn. 



GENERAL CONSIDERATIONS UPON NERVOUS DISEASES 



57 



Oppenheim's reflex is close to that of Babinski's. It consists of a 
dorsal flexion of the toes and foot when the inner surface of the leg 
is stroked from above downward. 

The comparative importance of the plantar over the palmar reflexes 
illustrates a cardinal law that is true of all the spinal reflexes appar- 
ently, namely, that the nearer they are to the brain, the less active 
they are. 

The presence of these skin reflexes leads to the inference, of 
course, that their arc through the cord is normal. Their absence, how- 
ever, does not signify very much, because the mind of the patient is 

FIGURE 2. 




Method of testing the patella reflex. 

so intimately implicated in them, that it is always a matter of uncer- 
tainty as to the physical or psychical cause for their non-appearance. 

Among the most valuable symptoms in neurology are the deep, 
tendon reflexes. It is not necessary to discuss here the many views in 
regard to their essential nature. Investigators of equal reliability 
hold that they are true reflex phenomena on the one hand, or mere ex- 
pressions of muscle tonus, itself a reflex phenomenon, on the other. 
For the clinician it is enough that they are regularly modified in dis- 
ease and that they represent a reflex impulse. 

The muscular contraction is provoked by a stroke upon the muscle 
or its tendon. The examiner's ingenuity will suggest Che best attitude 
of the patient for placing the muscle-tendon in a condition of slight 



58 



GENERAL CONSIDERATIONS UPON NERVOUS DISEASES 



tension withcut being pressed., stretched or otherwise prevented from 
acting. A slight blow with the percussion-hammer, or edge of the 
hand, will then cause the muscle to suddenly contract and throw out 
the limb. 

There are many conditions that might interfere w T ith the demon- 
stration of this phenomenon and of course they must be removed or 
given due consideration. The patient's mind may interfere. This is 
particularly the case in children. Hence distract their attention in some 
way or keep repeating the test while talking to them and in a moment 

FIGURE 3- 




Method of testing the patella reflex. 



of distraction it will suddenly appear. Disease states, in and about the 
related joint, in the muscles, and many other conditions, may interfere. 

As a general rule it may be stated that diminution or loss of the 
reflex means disease in the lower or peripheral motor neurones ; in- 
crease of it means disease in the upper or central neurones. In this 
way the deep reflexes become invaluable as localizing signs. 

In accordance with the muscle involved the symptom also helps 
us to localize the lesion in the segmental levels of the cord. 

The most important of the deep reflexes is that of the patella. A 



GENERAL CONSIDERATIONS UPON NERVOUS DISEASES 59 

child to be examined is placed on the edge of a chair ; an adult may sit 
upon a table. The legs are allowed to hang down at a right angle to the 
thigh. The examiner passes his arm under the knee of one leg and 
rests his hand upon the knee of the other. The patient is told to relax 
his muscles and to let his leg hang dead, as it were, and with full 
weight on the examiner's arm. I prefer this method to the common one 
of crossing one knee over the other in the ordinary sitting position. 
By the latter method there is sometimes considerable interference with 
the movement of the limb on account of the stoutness of the patient, the 
excessive tension put upon the tendon, or the occasional general incon- 
venience of the attitude. In the former method the patient can relax 

FIGURE 4. 




Method of testing the patella reflex with reinforcement. 

his muscles better, his mind is not centered upon the performance by 
the discomfort and the examiner can vary the tension of the tendon 
by slightly raising or lowering his arm. 

The tendon just below the front of the knee or just above it 
should be given a quick, sharp tap with the hammer or edge of the 
hand. The quadriceps femoris will then undergo a short, vigorous 
contraction and throw the foot out. If the patient ilexes and grips to- 
gether the fingers of his two hands, and then keeps trying to pull them 
apart, or if a child is given a small object to squeeze in either hand, the 
reflex response will be rendered considerably more distinct. This is 
what is known as reinforcement. 



6o 



GENERAL CONSIDERATIONS UPON NERVOUS DISEASES 



Apparatuses have been devised to measure the force of this reflex 
but they are too complicated for ordinary use and do not add much to 
the information when employed. 

The explanation of the phenomenon is that a genuine spinal reflex 
is present. The muscle — not the tendon and hence the error in the 
term tendon-reflex — is by the blow put into a state of sudden tension, 

FIGURE q. 




Method of testing the ankle reflexi 



myotatic irritability. An impulse rushes to and from the cord causing 
the muscle to undergo the sharp, quick contraction. Disease anywhere 
in the reflex arc therefore is indicated by diminution or loss of the 
jerk. I have once seen it absent in a woman who was apparently in 
perfect health and by reason of her early outdoor life enjoyed a vigor of 
physique above that of the average. Oppenheim says lie has known 
two or three such individuals. In a neuropath with various anomalies 
of developmentj be assumed that the absence o\ the knee-jerk was a 



GENERAL CONSIDERATIONS UPON NERVOUS DISEASES 



6l 



hereditary stigma degenerationis. These exceptional cases only prove 
the rule, that less of the knee-jerk means disease. 

Xext in importance among the deep reflexes is the ankle reflex 
and ankle clonus as it is called. The heel-phenomenon or Achilles ten- 
don reflex is constant in health and is well elicited by asking the pa- 
tient to kneel easily on a chair and then tapping the tendo Achilles. The 
-calf muscles contract and the foot is suddenly extended. This ankle 
reflex is much like the knee-jerk and is subject to the same general 
exceptions. 

The ankle clonus is a symptom of disease and never occurs in 

FIGURE 6. 




Mode of eliciting an ankle clonus. 

health. It can be elicited by suddenly or gradually putting the calf 
muscles under excessive tension. The patient sits down and extends 
his leg. The examiner grasps the foot and forcibly flexes it upon the 
leg. If clonus is present, it immediately begins to oscillate with rapid 
and regular and rather wide excursions. These oscillations usually 
number about eight or ten a second. They cease when the examiner 
lets go of the foot and the muscles are relaxed again. 

Though most of the authorities say that this is a phenomenon of 
the calf muscles, some recent investigations seem to point out quite 
definitely that it belongs only to the soleus and not to the gastrocnemius. 
This is in line with the fact long ago pointed out by Duchenne that in 
spite of their common insertion, these two muscles have distinct pur- 
poses. 

In hysteria and neurasthenia there is occasionally seen a slight, 
brief pseudoclonus. 



62 GENERAL CONSIDERATIONS UPON NERVOUS DISEASES 

A wrist reflex is obtained by stroking the tendons of the wrist 
when the hand of the patient is placed supine on the hand of the ex- 
aminer. A t^p on the styloid process of either the radius or ulna pro- 
duces the radial or ulnar periosteal reflex. 

Much more important than any of these among- the arm reflexes- 
is that of the triceps, which is elicited by letting the patient hang his 
forearm, while at right angles to his arm, loosely over the fingers of 

FIGURE 7- 




Method of testing the triceps reflex. 

the examiner and by tapping the tendon sharply just above the ole- 
cranon process. 

Bechterew has described a scapulo-humcral reflex. With the per- 
cussion-hammer taps are made along the entire inner edge of the 
shoulder-blade, and beneath the inner angle of the same. Especially 
marked is the response when the stroke falls on the inner edge of the 
scapula near the inferior angle. There is adduction and slight outward 
lotation of the corresponding humerus. 

Both a jaw reflex and a jaw clonus are observed. With the mouth 
held loosely open, the muscles relaxed as much as possible, a pencil* 
small ruler, or paper cutter is placed transversely on the lower teeth 



GENERAL CONSIDERATIONS UPON NERVOUS DISEASES 63 

and smartly tapped. The muscles of mastication contract, especially 
the masseters ; the jaw leaps upward. In disease when forcibly de- 
pressed a clonus or rhythmical up-and-down movement takes place 
in it. 

Among these deep reflexes must be included the pupillary and ac- 
commodation reflexes of the eye. A bright light focused into the eye 
causes the pupil to contract. If the patient is asked to gaze at some 
distant object and then at another object brought to his usual reading 

FIGURE 8. 




Method of testing the scapulo-humeral reflex. 

distance, or if he is asked to keep his gaze fixed on the examiner's 
finger as the latter is gradually carried towards his nose, the pupils 
will be seen to contract. Where the former or light reflex is lost, while 
the latter or accommodation reflex is retained, the pupil is referred 
to as that of the Argyll-Robertson type. 

The various visceral reflexes are of such familiarity tint scarcely a 
word need be said of them here. The vasomotor and secretory reflexes 
are visceral in a sense. Nausea and vomiting caused by rapidly re- 
volving objects before the eyes are of the same nature. The heart, the 
stomach, the liver, the kidneys, the rectum and bladder may all be 
affected by some form of remote sensory disturbance. We do not make 
use of these reflexes to -any extent in diagnosis. 

Idiopathic reflex irritability of the muscles is seen in neurasthenic 



6 4 



GENERAL CONSIDERATIONS UPON NERVOUS DISEASES 



and many other states. Diminution and increase of irritability are 
both observed. Percussion of the muscle awakens contractions that 
are lively and enduring, for a time. The same is observed when elec- 
tricity is the stimulant. In degenerative states both the mechanical 
and electrical irritability are usually reduced. 

When a muscle is suddenly relaxed and undergoes a slow tonic 
contraction, Westphal spoke of the condition as a paradoxical muscular 

FIGURE 9. 




Showing the mode of tt 



the jaw re Ilex 



contraction. It is best observed in the tibialis anticus when the foot 
is suddenly flexed on the leg. The mechanism is not known, nor arc 
we acquainted with its full significance. It is a rare phenomenon and 
never occurs in health. A somewhat similar exhibition has been seen 
in hysteria 

Electro-diagnosis in neurology is much more satisfactory than 
electro-therapy, in the fact that it is much more definite and accurate, 
And yet it is less resorted to than it should be, partly I suspect from the 



GENERAL CONSIDERATIONS UPON NERVOUS DISEASES 65 

fright produced in the minds of some by the vast array of symbols and 
formulae presented in certain works upon the subject. Neither the 
apparatus nor the principles upon which electro-diagnosis depends, are 
at all complicated. 

All that is needed in the way of proper paraphernalia are a good 
faradic battery, a good galvanic battery capable of furnishing a current 
of thirty or more milliamperes, a galvanometer for accurate measure- 
ments, though for general examinations even this is not necessary, 
good conduction cords, a rheostat and a number of electrodes of vari- 
ous sizes, in the handle of one of which is conveniently arranged a cur- 
rent interrupter. 

As time and space will be saved by the use of symbols, the follow- 
ing definitions are in order here. An will be used for the anode, or 
positive pole of the battery ; Ca will be made to stand for the cathode ; 
C is employed to denote a contraction of the muscle. 

CaCC in electro-diagnostic parlance means cathodal closing con- 
traction, which interpreted further means that, the anode being on some 
indifferent part of the body, when the negative pole is placed over the 
nerve or muscle to be examined there is a muscular contraction. 

In a similar manner CaOC is the formula for the contraction that 
would take place upon the opening of the current by removal of the 
negative electrode. 

AnCC stands for anodal closure contraction and AnOC for anodal 
opening contraction. To still further facilitate matters T is used to 
represent a strong continuous or tenatic contraction in the muscle, 
DeR the reaction of degeneration, and D the closed circuit or flowing 
current. Every examination for abnormality presupposes a knowledge 
of the normal. The same is true in electro-diagnosis. The normal 
polar formulae read thus : 

i. CaCC; 2- j InOC ; 3 ' CaOC ' 

These are varied and even reversed in disease. 

Moreover certain conditions must be observed and certain sources 
of error must be carefully avoided. 

Adults are more easily examined than children. In very early 
life, especially in the newborn, the skin, which is always highly resist- 
ent to the current is particularly so, and the peripheral nerves and 
muscles are incompletely developed. Adult results in electrical exami- 
nation are not observed in children until they are well along toward 
their fifth year. 

The resistance of the skin is overcome by moistening it and the 
electrodes freely with water in which a modicum of salt has been dis- 
solved. The passage of the current itself by stimulating the glands anil 
increasing the moisture of the skin in a few minutes increases the 
latter's conductibility. 

If one side of the body is diseased and to be examined, the other 
side should be simultaneously tested as a control. When both sides 
are affected resort must be had, unsatisfactory as it is, to a third per- 
son for the control tests. 



66 



GENERAL CONSIDERATIONS UPON NERVOUS DISEASES 



In adults, and especially in children, great care must be exercised 
not to confound voluntary and reflex movements with those produced 
by the electric current. The distinction can be detected by close 
watchfulness and frequent repetition of the tests. Allowances must be 
made for variations in the size of the electrodes used, the current 
being dense in direct proportion to its strength and in inverse propor- 
tion to the diameter of the electrode, and for such natural conditions 
as over-development of fat, etc. 

The limb to be examined should always be so placed that the 

FIGURE 10. 

(After Erb.) 



11. frontalis 
Oberer Facialisast 
U. coring, anpercil. 

M. orbic palpebr. 
Nasenniuskeln 

M. zygomatic! 

M. orbicul. oris 

Mittler. Facialisast 

M. masseter 

M. levator menti 

M. qnadr. meuli 

M. triang. menti 

Nerv. hypogloss. 

Unter Facialisast 

M.platysma myoid. 

Znngenbein 

muskeln 



11. omobyoideus 



N . thoracic, anter. 
til. pector.) 




W. pbreaicu 



Snpraclaviculax- 
pankt. (trb'scher 
Pnnkt. M. deltoid., 
biceps, bract ml. in- 
tern, n sopinaW 
long) 



Tlexu* 
bra 



Gegend d»r 
CeotralwioduBgco 



Gegeml d. 3. Stirn- 
windung n. Insel 
(Sprachcentiumt 

M. temporali* 

Ober. Faciatisast 
vor dem Obr 

N. facialis Stauiro) 
N. auricul. post 
Mitll. Facialisast 
Vnter. Facialisast 
M splemns 

M. sternocleido- 

mastoideus 
N. accessonus 
M. levator auguli' 

scapul 
M cucalaris 
N. dors, scapulae 



N. thoracic, long. 

(M. serratns aotic 

maj) 



effect of the stimulation can be easily manifested. A large electrode is 
thoroughly moistened and placed firmly against the lower part of the 
sternum. It is not to be moved during the entire examination. The 
other electrode, the small one with the interrupting attachment, is 
pressed firmly down, after having also been thoroughly moistened, on 
the nerve or muscle to be tested. 

The accompanying illustrations indicate the most favorable points 
at which to place this electrode to obtain the clearest responses from 
the respective nerves and muscles under examination. 

A weak current is employed first and then made stronger until 
there is a beginning twitch in the muscle. That indicates that the re- 



GEXERAL CONSIDERATIONS UPON NERVOUS DISEASES 



67 



quired strength of current has been attained. Each nerve of the limb 
should be examined above and below, using the points in the illustra- 
tions as guides. 

The first great fact to note in regard to the use of electricity for 
diagnosis is that it applies only to the lower or peripheral neurones. 
We can get no information of the condition of the upper or central 
neurones by the aid of electricity. Moreover, in regard to sensation it 

FIGURE 11. 

(After Erb.) 



If. tncepi (caput Ion gum) 

tt. triceps v caput intern ) 
A7r». ulnar ill 



M. fiexoi carpi olnaris 



M Sex. digitor. commun. 
profnnd. 



M. lex. dkrltor »oblira. 



M ilex. diglu»»bl (digit. 
indicii et minimi) 



Htn. utnaru 

M p.ilmaris bre? 

M. abductor digiti min 

M. flexor digit, inin 

M. oppoaene digit, min 



atst. lumbricalesJ 




H. deltoldeos 
(vord. Halfte) 



M. Uic9p» 
bracUii 



H. bracb. 
interuus 



M. supinator longns 
at. pronator teres 



at. flex, carpi radiaiU 

If. flex- digitor. eubliia. 

M. flex, pollicls longus 
Nerw. mtdianut 

M. abductor pollic. brer. 
M. opponene poUicla 

M. flex. poll. brer. 

JO, adductor pollic 



can afford us but very little knowledge that is at all definite enough 
to be of service. ' Therefore, electro-diagnosis is pre-eminently con- 
cerned with giving us information as to the condition of the lower 
motor neurones. In all diseases of the cord, the roots, and the nerves 
in which these neurones are implicated, electricity furnishes most valu- 
able diagnostic criteria. 

Let us now consider what are the normal and abnormal exhibi- 



68 



GENERAL CONSIDERATIONS UPON NERVOUS DISEASES 



tions. We have many distinct points of view from which to conduct 
the examination and mark the differences in the results. 

In the first place it should be noted whether the responses to any 
form of current are greater or less than normal. This is what is called 
the quantitative test. It is easily made and not of very great value 
in diagnosis. Mere increase or diminution of nervous irritability and 
muscular excitability, as we have already seen under the head of the 
reflexes, can be determined by mechanical means almost as well as by 
electrical stimulation. However, it is always wise to make the quan- 

F1GURE 12. 

(After Erb.) 



N. deltoideos (hinterr" 
HilfU) 



If. radialis 
M brachial, intern. 



M. supinator long 
11 radial, eit. long. 

M. radial, est. bre». 



it. extensor digit, f 
communis \ 



11. extenaor indicia 

M abductor pollic long. 
M. extensor pollic brer. 



U.lotero.i. dorsal. I 




JL trlcepi (caput longnm) 



liLtricepi (caput extern.) 



M. ulnar, extern, 
al. supinat. brer. 



M. extend, digiti 
M. eaten*, indicia 



M. extern. polL long. 



M. abdnrt. digit, mlw 

1 M. lntarojs. dormJ* 
I HI et IT 



titative tests and to record them with the galvanometer readings. Of 
course care must be observed to use always the same sized electrode, 
usually a small one, and to remember that normally different nerves 
and muscles differ in their quantitative responses. Stintzing used an 
electrode with an area of 3 sq. cm. Neglecting the muscle averages 
as of less importance, he found that for the nerves the averages were 
as follows, the galvanic being given in milliamperes and the faradic in 
centimeters on the scale attached to the sliding coil of his battery : 



GENERAL CONSIDERATIONS UPON NERVOUS DISEASES 



69 



Galvanic. Faradic. 

Ma. Cm. 

Facial nerve 1.75 121 

Frontal branch 1.45 128 

Mental branch 0.95 132 

Accessory nerve 0.27 137 

Median nerve (in arm) 0.9 122 

Ulnar nerve 0.55 130 

Musculospiral nerve 1.8 105 

Crural nerve 1.05 1 1 1 

Peroneal nerve 1. 1 115 

FIGURE 13. 

(After Erb.) 



M. adductor mtgnoj 
U. adduct longai 




V. thIm ioUrnu 



M. tensor fwciM l«tM 



it. qaidricips femorU 
(gemeinscbafU. Pankl) 



M recUt femoru 



U. tutus external 



Muscles vary more widely even than do the nerves. Even if we 
were to duplicate Stintzing's apparatus and methods in every particular, 
there are so many sources of error in the conditions of the skin, etc., in 
different people, that only wide variations from the above comparative 
figures can be taken as evidence of a pathological condition. 

Diminution in quantitative excitability is much more common, 
definite and available for purposes of diagnosis than is increase. In 
only one disease, tetany, does increase of excitability to the galvanic 
current figure prominently as a symptom. 

Much more definite and reliable are the qualitative changes 
that occur in the electrical responses as the result of disease. Here we 
have to consider the nature of the current, faradic or galvanic, em- 
ployed in the examination; the strength of the current; and the tissue 
undergoing the test, whether it is nervous or muscular. 

When for any reason a muscle or its nerve is severed from its 



70 



GENERAL CONSIDERATIONS UPON NERVOUS DISEASES 



nutrient center in the cell embedded in the anterior horn of the cord or 
cranial nucleus, it undergoes degeneration. This causes a change in 
the electrical responses. The result is spoken of as the reaction of de- 
generation and symbolized by ReD. It is obvious, therefore, that re- 
action of degeneration appears as a symptom in a great variety of 
diseases affecting the cells in the anterior horns of the cord and nuclei 
of the cranial nerves, the neuraxones belonging to those cells, and the 
muscles to which the neuraxones are attached. In such affections as 
poliomyelitis, the progressive atrophies of spinal origin, other diseases 
that damage the anterior cornual cells, bulbar nuclear paralyses, dis- 
eases that by compression or otherwise injure the anterior spinal roots, 

FIGURE 14. 
(After Erb.) 



I. tibial, antic 



ILextens. digit, comm. 
long. 



M. peronMaa breri* 



U extensor QiUociB 
long. 



Bm. InWiMMl donalM 




Ntrv. ptronaeut 



If. gestrocnem. extern. 
M. peromelia longu 



K. flexor htJlweU long. 



tt. extent, digit coma 
brent 



M. ebdnetor dlgiti min. 



and all severe degenerative diseases of the peripheral nerves like the 
infectious and toxic polyneuritides, ReD is a most important symptom. 
It never occurs as a sign of any affection that remains limited to the 
cerebral, upper or central motor neurones. In differentiating the two 
sets of paralyses therefore its value is obvious. 

There are various degrees of degeneration and the value of the 
symptom is furthermore emphasized in the remarkable fact that there 
is a direct parallelism between it and the degree of neuro-muscular 
degeneration. As the latter doesn't occur until about a week after the 
damage is first done, the electrical symptom will not be elicited be- 
fore that time. 

The immediate cause of the reaction of degeneration is the fact 
that the degenerated nerve terminals in among the muscle fibres re- 
quire a stronger and longer current than normal to excite them. 



GENERAL CONSIDERATIONS UPON NERVOUS DISEASES 



71 



As a very late phenomenon the same electrical manifestations may 
obtain in pure muscular affections wherein the muscular fibres are 
wasted. 

The reaction of degeneration reveals itself in two ways. There 
is a gradual loss of contractility to stimulation, and there is an actual 
change or reversal of the polar responses to galvanic stimulation. If 
the faradic current is employed, and first the nerve and then the mus- 
cle tested, it will be noticed that there is a gradual diminution of the 
rapidity and force of the contraction. In other words a stronger cur- 

FIGURE 15. 

(After Erb.) 



Hero ischiadic** 
K. bicepi fern. (cap. long.) 
K. bicepi fan. (cap. brer.) 



N prrontut 



al. gastrocnem. (cap. 
extern.) 



M. nuor'hallicU lOSgV 




f M. gluueus maxima* 



M. adductor magnoa 
M semiteadioosas 

SI. semimembranosus 



M. gulrocnem (cap. lot) 



M.. neior digitot. coma 
tongas 



rent of electricity will have to be employed to get a contraction anything 
near like that of the normal. Finally as the degeneration advances, no 
contraction whatever can be obtained, no matter what be the strength 
of the current that is tolerable. If regeneration occurs there is a re- 
turn of the faradic response in both the nerve and the muscle in the 
reversed order in which it disappeared. 

When the galvanic current is used and the nerve is tested the 
phenomena are about the same as they are with the faradic stimula- 
tion. In other words the galvanic excitability of the nerve is lost. If 
now the muscle be tested with the galvanic current, there is for a time 
a remarkable increase in the contractions or what is the same thing 
a weaker current is merely needed to awaken the normal contraction. 



72. GENERAL CONSIDERATIONS UPON NERVOUS DISEASES 

As the degeneration advances, finally the galvanic current loses its 
power of stimulation and then differs in no respect from the faradic. 
In regeneration of the nerve exactly the reverse order of events takes 
place until the normal status is reached upon the complete restoration 
to health. 

The following diagram will perhaps illustrate the characteristic 
features of the reaction of degeneration better than the above detailed 
description. It is taken from Erb to whom we owe much of our 
knowledge along this line. 

There is a change in the character of the polar responses also to 
galvanic stimulation of the muscles in the reaction of degeneration. 
The contractions are slow and worm-like instead of being sharp and 
lightning-like upon the closing and opening of the circuit. Moreover 
the normal superiority of the cathodal closing response over that of 
the anodal closing is reversed and the formula reads AnCC>CaCC. 
Even the cathodal opening contraction undergoes a greater in- 
crease than, and in very exceptional instances may even become equal 
to or stronger than, the anodal opening contraction. That these polar 
alterations are not as important reactionary signs of degeneration as 
are the differential phenomena between the faradic and galvanic re- 
sponses described above, is shown by the fact that we can even speak 
of the condition as a reaction of degeneration when the CaCC is 
equal to or exceeds still the AnCC provided the contraction is slug- 
gish in character. In some cases of partial reaction of degeneration 
there is a decrease of nerve and muscle irritability to both currents, 
whereas with direct stimulation of the muscle with the galvanic current, 
a slow contraction and reversal of the polar responses still obtain. 

The phenomena of the reaction of degeneration may be conve- 
niently summed up thus: 

1. Loss of nerve irritability to the faradic current. 

2. Loss of muscle irritability to the faradic current. 

3. Loss of nerve irritability to the galvanic current. 

4. (a) Early increase of muscle irritability to the galvanic cur- 
rent with later decrease, (b) Modification of the polar responses, 
even to the degree of complete reversal from those of the normal, the 
formula becoming AnCC equal to or greater than CaCC, with slug- 
gishness of the contraction as the most important feature of all. 

It may be mentioned that electricity is one of our best aids in 
detecting the feigning of disease, whether sensory or motor in type, and 
by it we can distinguish hysterical or pseudo-paralysis from the lower 
neurone types of organic paralysis. Consult the accompanying diagram 
for the best points to apply the poles. 

The vasomotor, secretory and trophic symptoms of nervous dis- 
eases call for but the briefest notice here as they are so generally local- 
ized in character that they can be better treated of under the head of 
brain and cord manifestations. 

The vasomotor and secretory phenomena are very closely inter- 
related and are supposed to be largely under the control of the sympa< 
thetic system. 

Flushing and pallor of the skin and mucous membranes, local and 



GENERAL CONSIDERATIONS UPON NERVOUS DISEASES 



73 



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74 GENERAL CONSIDERATIONS UPON NERVOUS DISEASES 

general, may be frequently observed. Sometimes they can be elicited 
by causing a mental shock to the patient or by irritating the skin. 
Dermographia is where one can write with the back of his nail on 
the patient's skin and the tracing remains a long time. The tdche 
bleuatre of the French authors is an unimportant vasomotor manifes- 
tation in the skin. 

Any of the secretions may be increased or diminished. This is 
usually due to associated vasomotor trouble. Special names are em- 
ployed for the various forms and localizations of the secretory exhibi- 
tions. They are such as hyperidrosis and anidrosis for disturbances 
of the perspiration ; salivation for increase of the saliva ; diuresis for 
excessive flow of urine. 

The trophic symptoms are usually due to spinal disease and will 
be described at the head of those troubles. True atrophies must be 
carefully distinguished from pseudo-atrophies due to non-use. True 
hypertrophies and pseudo-hypertrophies must be carefully differen- 
tiated. The former must not be confounded with enlargements from 
other adventitious causes of enlargement. A hypertrophic joint for 
instance is not the same as a swollen and ©edematous joint. 

Trophic disturbances can be observed in any or all of the tis- 
sues of the body but they are extremely obvious at times in the epi- 
blastic elements such as the skin, the hair, the nails, etc. 

Ulcerations, pigmentations and many other changes are observed 
in the skin as a result of its diseased innervation. It is beginning to be 
recognized that many skin affections are really nervous troubles. 
Herpes, urticaria, scleroderma, pemphigus are neurotic in origin. 
General trophic diseases like arthritis deformans are, in some 
cases at least, of the nature of trophoneuroses. Just how the nervous 
centers preside over the nutrition of the body we do not clearly know ; 
whether their influence is direct or indirect, whether it is physical or 
chemical. We do know, however, that most important trophic centers 
are located in the gray matter of the spinal cord and that they oper- 
ate upon the tissues largely through the sympathetic and spinal nerves, 
together or separately. 

Trophic symptoms need no tests as they are wholly a matter of 
observation. The trophic changes in the muscles are accompanied by 
the peculiar phenomena described under the reaction of degeneration 
in the paragraphs devoted to electro-diagnosis. Trophic skin changes 
are less responsive to local medication than are those due to inflam- 
matory troubles, and this sometimes aids in their diagnosis. 

The visceral symptoms of neurology are motor, sensory, secretory 
or trophic in character and may therefore be passed here. They arc 
important, however, and should always be carefully noted in the ex- 
amination of every case. 

Local thermometry is sometimes a valuable assistant in diagnosis. 
The vasomotor condition, inflammatory or spasmodic, usually under- 
lies it. Thermometers of various types have been devised for resting 
against the head and elsewhere. Tumors and abscesses of the brain 
and focal inflammations have sometimes revealed spots of slightly 
altered temperature in the scalp. The same has been less frequently 



GENERAL CONSIDERATIONS UPON NERVOUS DISEASES 



75 



observed in severe, focal cord troubles. The findings, however, are 
not sufficiently uniform or definite to make them very satisfactory as 
diagnostic criteria. 

General thermometry is the same in nervous as in other forms of 
infection and inflammation. 

The pulse may be due to a vasomotor disturbance ; otherwise it 
follows the same laws that it does in other pathological states of the 
.general organism. 

Skiagraphy, or shadow pictures made with the Rontgen ray, has 
added a most valuable aid to the diagnosis of some superficial and 
even deep lesions in the nervous system. Bullets and other missiles 
have been located by this method. Exostoses, spiculse, depressions and 
fractures in the inner table of the skull have been thus discovered when 
there were no external signs of any sort. Many tumors and growths 
can, if not too deeply buried, be thus outlined. Cortical growths are 
especially discoverable by skiagraphy ; basal growths are perhaps the 
least so. 

The examination of the cerebrospinal fluid and the value of the 
findings will be referred to again under the head of lumbar puncture in 
the chapter given to the anatomy of the spinal cord. 

GENERAL CONSIDERATIONS UPON THE TREATMENT OF 
DISEASES OF THE NERVOUS SYSTEM. 

I hesitate very much to write the following chapter, because liter- 
ally there are no general principles of treatment that apply to all pa- 
tients alike. Human beings are not automata nor machines built upon 
exactly the same plan and with the same measurements. Each in- 
dividual has his own peculiarities, so that it becomes literally true what 
is one man's meat is another man's poison. In the nervous system, 
wherein resides the very center of the individual's personality, the 
constitutional and functional differences between men are more marked 
than they are in the other organs of the body. The nervous system is 
the immediate source of all human activities. From the creation of a 
Paradise Lost to the sweeping of a public highway, the nervous system 
is the beginning and source of the phenomena. All other organs de- 
velop and functionate nearly in the same way in all men. but in regard 
to their nervous functions the differences are enormous. It is the fail- 
ure to recognize this fact that leads to so much dissatisfaction in the 
management of these affections. The greater the need of individualiz- 
ing in any kind of work the more patience, thought and concentration 
is demanded of the worker. It is much easier to think mechanically 
and machine-like, to have a single formula by which to treat all hys- 
terias alike and another by which to label always certain general 
groups of symptoms by a given name. It saves time and the expendi- 
ture of mental force. But, alas! it is usually disastrous to the patient's 
welfare and to the physician's reputation. Under such circumstances 
the former usually turns to quackery, while the latter rails at the hor- 
r< rs of nervous diseases. 

It is notorious that in general practice pessimism in regard to the 



j6 GENERAL CONSIDERATIONS UPON NERVOUS DISEASES 

prognosis of these affections, and nihilism in regard to their treatment 
are all too common. The reason for this is often too obviously in the 
temperamental and mental inadequacy of the practitioner. He either 
lacks the proper amount of patience, his trend of thought is too mechan- 
ical, he is mentally lazy or he is ill-informed in regard to the newer 
discoveries in neurology. 

I was recently asked by a gentleman of large practice what a 
neurone was ; another informed me that hysteria was nothing but 
devilishness in the woman ; a third wanted to> know what I usually 
prescribed for paralysis ; while a fourth emphatically declared there 
was no such thing as neurasthenia. 

Such exhibitions make one feel that there are worse things than 
nervous diseases, and chief among them are the dogmatism of ignor- 
ance and the assumption of egotism. 

On the average the prognosis and treatment of nervous diseases- 
are about the same as they are in other troubles. All of the self- 
limited infections are beyond the pale of cure in the sense of ceasing at 
the behest of the physician. The latter merely controls their symp- 
toms, wards off complications and helplessly lets them run their course 
and terminate themselves. We can do pretty nearly as much as that 
in locomotor ataxia and a great deal more in brain tumor. If hys- 
teria is incurable, and can only be controlled when it breaks out in 
exacerbations, as it were, what are we to say of the rheumatic diathe- 
sis, of gout, of diabetes and the other constitutional diseases? Is val- 
vular disease of the heart ever cured, or advanced pulmonary tuber- 
culosis, or certain forms of renal disease ? 

As among other affections so among the nervous, we have the in- 
herited, congenital and constitutional troubles that can only be con- 
trolled and treated symptomatica! ly, whose course is chronic, and 
whose termination is only with death. 

On the other hand, there are many acquired diseases, like chorea, 
neurasthenia, syphilis of the central nervous system, multiple neuritis, 
that give most brilliant results under proper treatment. 

A pessimistic view of neurology is unwarranted and exposes the 
holder of it to the charge of being too badly informed to make an ap- 
proximately correct diagnosis, too inappreciative of the close relation- 
ship of the nervous system to the personality of the patient, too gross 
and mechanical in his mode of thinking, too empirical in the use of 
his remedial agents, and too oblivious to the important distinction be- 
tween inherited and congenital unalterable disease states and alterable 
and acquired temporary states. 

The purpose of this chapter will be to point out a few general 
principles of neurological therapy in order to more particularly empha- 
size the unreasonableness of therapeutic nihilism. It is most assuredly 
not written to enable any one to concoct a fixed scheme of treatment 
for all cases of nervous disease alike and thus to shirk the labor and 
responsibility of studying and managing each individual case upon its 
own merits. 

There are three prominent indications in the treatment of nervous 
disease. 



GENERAL CONSIDERATIONS UPON NERVOUS DISEASES JJ 

In the first place, the prevention of the disease itself, its return, or 
its exacerbation should always be attempted by the aid of proper 
hygienic and prophylactic measures. 

In the second place, every endeavor should be made to remove 
or render inactive the cause. 

Thirdly, the symptoms should be controlled in the hope of thereby 
removing their cause, or at least of mitigating the distress produced 
by them. 

In striving after these various ends we find that we have at our 
disposal various classes of agents. They are the psychic, the physical 
and the medicinal. I include surgery among the physical measures. 

Psychic, physical and even medicinal means may have to be em- 
ployed in the prophylaxis. The putting of an individual into the best 
condition to ward off disease means the putting of him into the very 
best mental and physical hygienic state. Mind and body must be 
trained to make for health and not for disease. Good physical and 
mental food is a necessity. Proper and varied exercise is a prerequisite. 
Cleanliness, system, regularity, moderation, serenity and freedom from 
irritation and exhaustion are desiderata. Ignorance of the laws of 
health is not so widespread as indifference to them. Ignorance in re- 
gard to the dangers of their infraction is the cause of much of this 
indifference. It becomes the duty of the physician, therefore, to warn 
as well as to instruct, to arouse by awakening alarm as well as to 
calm by conveying correct information. In doing thus his duty he may 
have to touch upon every minutia in the diet, the clothing, the habits, 
the occupations, the amusements, the mentalization even of his protege. 
Nothing is too insignificant in the prophylaxis of nervous diseases. 
Much of the advice w T hich he is to give is commonplace and well known, 
but people are thoughtless and forgetful and he has assumed the role 
of conservator of their health ; it behooves him, therefore, to iterate 
and reiterate his injunctions, however trite they may seem to be. 

One of the most important questions, though unfortunately not 
one of the most frequent, that he will be consulted upon is that of 
marriage and the possible effects of heredity. In no branch of medi- 
cine is heredity so prominent a factor as in neurology. Heredity is a 
tremendous feature in etiology. In the prevention of these troubles 
it must receive high consideration. If not for their own good, at 
least for the good of society and future generations, the unfit should 
not marry. It would lead me too far to mention all the forms of 
nervous disease that ought to restrain those contemplating marriage 
from that which will most assuredly give to the world more defective 
and more diseased offspring. The intermarriage of near blood rela- 
tions should be interdicted. Two nervously afflicted individuals should 
not enter into wedlock. An individual who has a form of nervous 
trouble in which heredity is recognized as a marked element ought not 
to beget children. Syphilitics should not marry. Members of fami- 
lies in which there is a clear psychopathic taint would not marry if 
they considered the welfare of others besides themselves. Members of 
families in which there is a traceable neuropathic taint should be slow 
about contracting union, or if they do marry they should unite in a 



yS GENERAL CONSIDERATIONS UPON NERVOUS DISEASES 

family where there is a history of exceptional health and vigor for 
several generations back. The children of a neuropathic ancestry 
need close observation, but coddling should be most strenuously guard- 
ed against. These children are ofttimes unfortunate in being the vic- 
tims of both a bad heredity and a bad discipline. They are sometimes 
brilliant, precocious, entertaining and physically weak. They are the 
center of the family interest and sympathy. They are therefore over- 
indulged, injudiciously humored and spoilt. Their physical and mental 
lives are all but riotous. They live as they please, eat as they please and 
think as they please. The consequence is inevitable. On the other 
hand, I sometimes wonder if it is not a greater evil to be the child of 
self-opinionated, narrow-minded, ignorant disciplinarians. I am con- 
vinced that in too many cases not neglect and overindulgence are the 
bane of these children so much as too much regulation — nagging, in 
fact — by anxious and loving but woefully stupid, ill-informed and 
short-sighted parents. I have frequently seen young neurotic girls 
driven almost insane by the imperious attentions of a mother who 
meant well, but who was incapable of seeing things from her daugh- 
ter's point of view. A school for parents would be a godsend for many- 
neuropathic children and its curriculum would include training in what 
not to do as well as in what to do. 

These children of neuropathic parentage need, as a rule, sys- 
tematic, wholesome, evenly balanced lives. All shocks, unusual or 
one-sided strains, freakish habits, intemperance in thinking, in eating, 
in drinking and in everything should be prevented. A steady moral 
purpose in life, a wholesome ambition in some one direction and a 
good regime in living should be inculcated. Nerves are marvelously 
built up and kept strong by systematized and regular mental and physi- 
cal activity. 

The same applies to adults as to these children. Dissipation, 
irregularity, extremes are disastrous to the health of the nervous tis- 
sues. Proper exercise of the entire personality, mental and physical, 
in a manner conducive to a well-balanced organism is a necessity. 

It is more solacing, but less truthful, to say that hard work is the 
cause of much modern nervousness than it is to say it is due to the 
distractions, dissipations, fuss and fume that are allowed to accompany 
the hard work. Hard work may injure its hundreds, but excessive, 
purposeless motility, mental flightiness, silly rush and roar, false and 
foolish identifying of mere mental and physical bombast with real ac- 
complishment injures its thousands. 

The use of alcoholics, tobacco and noxious beverages, the diet and 
the mode of eating it, the frequency and the style of bathing, the hours of 
sleeping, the whole life of the adult must be inquired minutely into, 
and proper suggestions made along well-known lines to insure against 
the outbreak of a possible or threatened nervous affection. 

The dietetics of nervous diseases has its greatest field of operation 
in neurasthenic and allied states. As I have treated of the subject in 
detail under the head of neurasthenia, I will not speak of it further 
here. It should be noted, however, that for neuropaths generally a 
wholesome nitrogenous diet, with the drinking of abundance of water 



GENERAL CONSIDERATIONS UPON NERVOUS DISEASES 79 

between meals, is to be employed. It includes meats, fowl, fish, eggs, 
milk, buttermilk, green vegetables, bread and butter. As a rule I find 
that neurotics do not eat enough or too much of some particular sort 
of food. Especially fats do they seem to eschew. They overindulge 
in stimulants, tea and coffee. I am convinced that in these cases it 
is not so important to advise a selected diet as it is to urge a generous 
one. Whims and notions often confront the advice of the physician, 
and if he pays much attention to them he will have to change the 
dietary every few days. I therefore try to discover, after a short period 
of observation, about what agrees best with the patient apart from any 
notions that he may himself have. I then urge that this food be taken 
in large amount, in several small meals a day if necessary at first. 
Even less digestible food is better for neurotics than little or no food. 
The stomach can always be assisted in the disposing of it with proper 
agents. 

Food, then, the best, the plainest and the most wholesome if possi- 
ble, but always food, more food, should be the guiding suggestion in 
regard to the dietary of most nervous people. The exceptions are 
relatively few and capable of being easily met. 

Athletes are not, as a rule, good brain workers, nor, on the other 
hand, is it necessary for people whose nerves are under a high tension 
to strive to become athletes in order to preserve health. It is amazing 
the amount of ignorance there is among the laity in regard to the mat- 
ter of physical exercise. Unused muscles, of course, with an over- 
worked brain produce an unbalanced organism. A certain amount of 
exercise, therefore, is absolutely imperative. Among real brain workers 
there is not enough exercise taken, as a rule, and among a large class 
of pseudo-brain-workers there is entirely too much exercise indulged in. 

No exercise is of much benefit that fails at the same time to inter- 
est the mind. To wearily stand and swing dumb-bells or Indian clubs 
in a close, stuffy gymnasium in the hope of gaining health is almost 
ludicrous. Long forced walks in which one is longing all the while to 
return home are not conducive to health. Such exercises merely weary 
the muscles and depress the mind. It is my observation that in a good- 
ly proportion of cases too much mere physical exercise is taken. I am 
often consulted by persons who are on the verge of profound nervous 
collapse and yet who wearily force themselves every day to take a 
cold plunge bath and a monotonous measured walk. What such per- 
sons need is usually rest and less task-work ; in a word, very moderate 
exercise with plenty of amusement. 

And this leads me to state another point I also believe to be true, 
namely, that many business men who are monotonously confined to 
their offices all day do not need physical outdoor exercise so much as 
they need relaxation and change of brain activity. The grind of busi- 
ness develops but one side of their mental faculties. They need, there- 
fore, psychic change even more than physical change. All sorts of 
outdoor games and sports are commendable therefore. Moderation 
should be the rule always even here. 

The bath is a powerful agent for good or for evil, hence the ground 
for the extremists who on the one hand spend half their lives in water, 



80 GENERAL CONSIDERATIONS UPON NERVOUS DISEASES 

or on the other indulge in the luxury once in two or three years. Here 
as everywhere moderation and good judgment are necessary. 

Cleanliness is, of course, next to godliness and should be a law ; 
but except under some special conditions -it is not necessary to spend 
the greater part of one's existence in the bathtub to keep clean. I am 
of the opinion that many people bathe overmuch as well as that many 
bathe not enough. Here again each one must be a law unto himself. 
As the bath is, by reason of its delightful after-effects, a sort of luxury 
as well as necessity, it can easily be overindulged in. 

Human beings are not water animals. I know of instances where 
the frequent and prolonged immersion of the body in water, the over- 
stimulation and excitement induced in a delicate organism by too fre- 
quent cold plunges, the tenderness and enervation fostered by too much 
employment of the hot water, and above all by too frequent rasping of 
the skin with harsh brushes, rough towels and dirty soaps, have done 
positive harm, though the practice had been persisted in because it gave 
a temporary pleasant feeling and held out a fatuous hope of increased 
health. Therefore, while a daily bath is to be commended, it is to be 
adjusted to the individual. His constitutional needs, his power of 
reaction and his general vigor must be taken into account when the 
questions are raised as to the frequency of the bath, the proper tem- 
perature of the water, the duration of the immersion and the various 
after procedures. Remember, too much and injudicious bathing are as 
harmful as too little or none at all. 

When a physician is consulted by an individual who already mani- 
fests the symptoms of a definite nervous trouble, it becomes his first 
duty to search for and remove, if possible, the cause. This may tax his 
ingenuity to the utmost and call upon all of his mediate and immediate 
resources. All of the therapeutic forces may have to be brought into 
play here to banish the cause of the disease, as well as the disease 
itself. Psychic, disciplinary and pedagogical measures can remove a 
false mentalization which underlies some cases of the psychosis hys- 
teria. A calming manner, an assurance that everything is all right, 
an assistance on the part of the physician in banishing trifling worries 
and at times an autocratic severity with positive commands, will do 
more than bottles of medicine. A weak personality, a hesitancy and 
uncertainty begotten of want of knowledge, or an exposure of the fact 
on the part of the attendant that he is not perfectly master of the sit- 
uation will be sure to heap trouble upon trouble for him and will send 
the patient's symptoms into an exalted degree of manifestation. It is 
the difference between doctors themselves in this respect that often 
causes the apparent differences between patients in regard to their 
responsiveness to treatment. This is so strikingly true that it under- 
lies the wide variations of opinion among medical men in regard to 
nervous diseases and their management. It is so true that a practitioner 
who finds he is mentally set all awry and meets with constant discour- 
agement in his neurological practice, whose cases go to his rivals and 
remain under their treatment and even get well, will do wisely to blame 
himself and endeavor to find out and correct his own shortcomings. 

Change of environment, change of companionship, change of 



GENERAL CONSIDERATIONS UPON NERVOUS DISEASES Si 

thought, suggestion, and even occasionally hypnotism, may have to be 
resorted to in order to lift the patient out of the mental state upon which 
his psychosis and neurosis may largely depend. 

The physical causes of nervous diseases are so numerous and 
the methods of attempting their removal are so commonplace that noth- 
ing but a bare mention of them need be made here. There are the 
intoxications, for instance, such as alcohol, arsenic, lead, morphine, 
cocaine; the infections, like syphilis, tuberculosis, pneumonia, malaria, 
influenza. These will all have to be attended to and removed before 
their nervous sequelae can be expected to mitigate. 

Surgical treatment will be called for in removing distant sources of 
infection, like abscesses. Tumors and deformities and exostoses press- 
ing upon the nervous tissues will demand the first consideration. I 
have seen simple lateral curvature uf the spine cause a severe hystero- 
neurasthenic condition. The dependence of Jacksonian epilepsy upon 
injuries to the skull is well recognized in some cases. The origin of 
intracranial abscess from mastoid and ear disease is all but universal. 

Many nervous diseases need no further treatment than simple re- 
moval of the cause. It is positive malpractice to go on plying the pa- 
tient with analgesic and antispasmodic remedies without attempting 
to discover and remove the cause. Only when the latter is absolutely 
impossible is symptomatic treatment justifiable. 

The symptomatic therapy as applied to nervous diseases involves 
psychic, physical and medicinal measures. 

I have already referred sufficiently to the general psychic influ- 
ences, which are the same here as they are when employed in the pre- 
vention of disease. Suggestion and hypnotism will be treated of more 
in detail in another part of the volume. I will mention here, however, 
that psychotherapy is of wide application and includes much more 
than is usually credited to it. I do not refer to direct psychotherapy, 
for that is acknowledged by every one to be a powerful weapon against 
diseases of a certain order. AYhat I mean to say is that even indirect 
psychotherapy is frequently quite as forceful in accomplishing good. 
I am convinced that not a little of the benefit obtained by both physical 
measures and drugs is due in some cases to the change of mentaliza- 
tion which they indirectly induce in the patient. Metallotherapy, elec- 
tricity, massage, mechanical exercises, baths are almost as efficient in 
affecting the patient's mind, in awakening new hopes, in dispelling 
despair, apart from their mere physical effects, as is music or change 
of companionship or general environment. In fact, they constitute a 
part of the change of environment and as novelties cause a novel train 
of thought. They are all legitimate means to use, in properly selected 
cases, for their psychic as well as for their physical influence. 

The physical agents at our disposal include those of hydrotherapy, 
me chanic other apy, electrotherapy, massage, gymnastics and surgery. 
To treat exhaustively of any one of these would take more space than 
can be allotted here and the reader is therefore referred t<> the numer- 
ous special treatises upon them. Some few general principles may 
not be improperly enunciated, however, at the beginning of a volume 
upon nervous disea 



82 GENERAL CONSIDERATIONS UPON NERVOUS DISEASES 

There are many kinds of baths in vogue to-day for the treatment 
of disease, as, for instance, the water, the electric and the light baths. 
Even mud, paradoxical as it sounds, is now the constituent of a bath. 

Hydrotherapy means the employment of hot and cold water to 
stimulate, quiet and otherwise modify the functions of the nervous 
elements. The ice bag is to be included, as that is a sort of local appli- 
cation of cold hydrotherapy. 

There is much refinement, some of it unnecessary in my opinion, 
in the division and subdivision of baths in works upon hydrotherapy. 

Two great forces underlie all forms of the therapeutic use of water 
in this way. One is the thermal force, the other is the mechanical. To 
be sure, they are practically both the same, for thermal force is believed 
now to be due to the mechanical activity of molecules. 

The modes of applying hydrotherapy involve the consideration of 
the application to and the abstraction from the body of heat, and stimu- 
lating, benumbing and other effects produced upon it by the weight, 
force and shock of the water. As a general rule cold baths, however 
applied, are stimulating. If too long in duration or if the patient's 
reactive powers are weak, stimulation passes over into exhaustion. 
Cold baths are not tonic in the sense that they are frequently supposed 
to be. If brief and employed in persons of vigorous constitution, they 
first contract then dilate the peripheral vascular apparatus. This sends 
the blood bounding through the body and hastens all the vital processes ; 
hence the exhilaration that usually succeeds a plunge into a tub of 
water at 60 or 70 degrees F., followed by a brisk rub. In a way a bath 
of this sort is like all other stimulants, even alcohol. It is not a tonic 
per se. It uses up quickly pabulum, it heightens all of the tissue ac- 
tivities, it excites into exalted power the vital organs, it enlivens the 
whole being even as alcohol does. 

The value of such an agent is incalculable, but, like a double-edged 
sword, it can cut both ways. It is pitiful to see how often nervous sys- 
tems that are worn out and in need of rest, that are crying loudly for 
more nourishment and less stimulation, are whipped up by all sorts 
of irrational methods of cold bathing. Great harm has been done, 
I am certain, by the promiscuous use of the cold bath, and all of its 
variations, in neurasthenia and other states of depression in which 
malnutrition is a prime factor. 

The mechanical effect of the water is added to that of the cold by 
applying the bath in the form of a shower, a solid jet (Charcot douche), 
a rain or a rapid spurting. Alternation of a hot and cold jet thrown 
against the body from a distance of ten or twelve feet constitutes the 
Scottish douche. Other modes of applying cold hydrotherapy are the 
wet sheet, the cold compress, the cold rub, the cold pack and the ice 

ba s- 

As a general rule all such applications, even the full or partial cold 
bath, should be brief and followed by thorough drying and toweling 
to provoke a reaction. Two per cent, of brine may be judiciously added 
to the water sometimes, thus simulating it to a natural sea bath. Many 
of the medicinal springs where baths are employed owe their virtue to 
the coldness of the water. 



GENERAL CONSIDERATIONS UPON NERVOUS DISEASES 83 

Extremely hot baths may be stimulating, but warm baths as a 
rule are sedative and tonic. The temperature of the water should be 
from 90 to 100 degrees F. Full baths, partial baths, sitz and foot baths, 
hot wet packs, hot compresses, sprays, douches, fomentations and hot 
water bottles are some of the ways in which heated water may be 
employed. In the Turkish bath the body is first exposed to a dry tem- 
perature anywhere from 130 to 200 degrees F., and then plunged into 
cold or gradually cooled water. In the Russian bath steam vapor is 
used and with higher temperatures even than those of the Turkish 
bath. A method of applying heat locally dry, even to the height of 
400 degrees F., is by means of Beck's various apparatuses. The virtues 
of the hot mud, sand and other baths, as well as those of hot springs 
geaerally, are due entirely to the heat. According to the degree of heat 
there is first a contraction then a dilation of the peripheral circulation, 
which, however, lasts longer than it does after the cold bath. The 
sensibility is lessened and hence hot baths are sedative in irritable and 
painful states. A feeling of complete relaxation, languor and sleepiness 
usually follows them. The metabolism is slightly increased and the 
urea is more freely excreted. The pulse and respirations are at first 
rendered more rapid, but they soon become calm and steady. As a 
sedative, therefore, a warm bath is most valuable. In its power of 
provoking gentle and prolonged increase of the vital forces without 
causing excitement and high stimulation, the warm bath is more tonic 
than the cold. If it is taken too frequently, however, too hot or too 
long, it is enervating. As a continuous therapeutic measure it is more 
generally useful than cold baths in weakened states. Its effects may 
not be so immediately noticeable, but they are more lasting and 
nutritional. 

Mec hemic 0- therapy, massage and passive and active gymnastics 
all belong to the same general category. The basic principle underly- 
ing them is muscular and vasomotor movement by compression, irrita- 
tion and stimulation. The variations upon the principle are innumer- 
able and involve all sorts of mechanical methods and contrivances. 
Exercise, local and general, passive and active, is the foundation of 
these muscular methods of cure. In various institutions throughout 
the land are elaborate machines whereby patients are rubbed and 
shaken and twisted and slapped and punched and rolled and vibrated, 
until one wonders whether human beings after all are nothing but 
masses of impressionable dough. One cannot entirely gainsay these 
methods, elaborate and ludicrous as they sometimes are. In supplying 
that which the mental inertia of the patient himself makes wanting, 
they do indeed somewhat stimulate the organs and tissues of the body. 
Like the Kentucky colonel's infallible cure for a bad liver — namely a 
ride on a bad saddle horse — they do shake one up, and even a shake has 
its advantages. One wonders what sort of a pathology, except that 
which goes with natural laziness and acquired aboulia. is that which 
can he cured by shakes and slaps. ]f the patients enjoy it, however, 
and their faddish propensities are satisfied, we can at least attribute a 
large amount of the benefit to the psychic effect. Much of the talk- 
about the dissolution of adhesions, of the absorption of adventitious 



84 GENERAL CONSIDERATIONS UPON NERVOUS DISEASES 

matter and the revivification of the tissues is the mere twaddle of ad- 
vertisement and has no basis in fact. Massage and gymnastics are 
real and valuable aids in the treatment of nervous troubles and so far 
as the steam-engine, mechanico-machine methods can be made to imi- 
tate intelligent massage and normal gymnastic movements they are 
not to be condemned. 

Massage is a local exercise of the muscles entirely passive in char- 
acter. It has been systematized and more or less elaborated. In pro- 
voking fine muscular movement, in eliminating local products of 
metabolism and in hurrying on the flow of the blood current it lends 
itself powerfully to the relief and cure of nervous diseases. By blunt- 
ing the sensibility it relieves pain, warmth is created in the muscles and 
on account of the circulatory phenomena in them the latter maintain 
their normal development. 

Massage should never be employed except with a full realization 
of the underlying pathological condition and the end to be attained by 
it. In applying it the hand or hands of the operator, previously oiled 
with olive or cocoanut oil or not, are used and the strokes are always 
made toward the heart or centers of the body. In a general massage it 
is always best to begin at the periphery and work towards the body. 
The movements consist of gentle, steady, regular rubbing, pinching, 
squeezing, pressing, kneading and rolling of the muscles always in one 
direction. The pressure may be gentle or firm, superficial or deep, 
brief or prolonged. The patient, of course, remains all the while abso- 
lutely quiet. 

Gentle stroking or effieurage is perhaps the most generally used 
manoeuvre to begin with. It consists of quickly and lightly tapping the 
muscle. When the strokes are more energetic with one hand, while 
the other hand rubs the surface to and fro, the process is called massage 
a friction. 

Tapotement or percussion with the fingers and kneading are a 
couple of the frequent ways of employing massage. 

The patient must never be wearied by the treatment. As a rule 
a seance need rarely last longer than a half or three-quarters of an 
hour, often much less. Usually a restful and relaxed feeling follows. 
If the patient is inclined to sleep, he should be encouraged to do so. 

It is a good thing to give the massage usually after the morning 
bath. It should not be employed too soon before or after a meal. If 
given in the evening it is liable to disturb the night's rest. 

Gymnastics are active or passive. This is not the place to give 
an elaborate description of them. Passive movements of all sorts may 
be given while the patient is in or out of bed. He may or may not be 
told to resist the operator. 

Szvedish movements are of the nature of gymnastics. 

Active gymnastics, calisthenics are all well known and need but 
to be mentioned here. The use of rubber bands, dumb-bells. Indian 
clubs are advantageous at times. Moderation, gradual increase, en- 
tertainment and plenty of good fresh air must be enjoined while under- 
going gymnastic treatment. As soon as possible die patient should 



GENERAL CONSIDERATIONS UPON NERVOUS DISEASES 85 

leave gymnastic exercise for the final and more natural exertions that 
accompany outdoor walks, games and sports. 

For a discussion of the nature of electricity, the apparatuses em- 
ployed in its generation, and the laws in regard to its physics the reader 
should consult special works upon the subject. Here only a brief 
outline of its use in therapeutics can be introduced. 

There is much glamor surrounding the subject of electrothera- 
peutics and much mystery kept alive by the use of a lot of unnecessary 
details and formulae. Not so much harm is done by the want of knowl- 
edge in regard to volts and ohms and watts and electromotive force 
as by the inability to make a sufficiently correct diagnosis so as to 
know when and when not to use the electricity. As a natural force it 
is the same always, however it may be generated. The strength and 
character of the current are variously modified so that a slightly differ- 
ent effect is produced upon the tissues by these variations. 

The necessary electrical outfit for neurological work is not elab- 
orate. As a part, and a large part in my judgment, of the benefit of 
electrical treatment is to be attributed to its psychic effect, an elaborate 
display of apparatus has its advantages. The physician may, if he 
chooses, imitate the quacks and obtain some of the good results which 
they thus sometimes obtain. For actual physical electrotherapeutics, 
however, as I have said, not much of an apparatus is needed. 

The first requisite, of course, is a good generator of the electricity. 

Static electricity is obtained from the well-known static machine. 

Faradic and galvanic electricity are secured from the zinc-carbon, 
the dry silver-chloride or other form of galvano-faradic battery. In an 
office illuminated by electric light the electricity may be obtained by 
tapping the wires and using the commercial current after it has been 
passed through and is under the control of an appropriate rheostat. 
A milliampermeter is necessary to measure the dosage, and various 
electrodes and an insulating stool with the static machine, are needed 
to administer it. All kinds of ingenuity have been displayed in the 
creation of electrodes. What will be actually needed, however, are a 
couple of plain handles, one about 10 cm. and the other about 40 cm. 
long, a third handle with an interrupting attachment to it, an electrode 
about 5x15 cm. square, another about 10 sq. cm. in area, and a third 
about 1 sq. cm. A soft wire brush and a rheostat should also be among 
the fixtures. With most static machines a regular set of electrodes is 
furnished. High frequency currents, now being used with some degree 
of success, as well as the X-ray, need special apparatus. 

Perhaps a few definitions here of electrical terms may be allow- 
able. The anode is the positive pole; the cathode is the negative. A 
current is spoken of as stabile when the electrode is held steadily in one 
place, as labile when it is rubbed or moved over a part. An ascending 
current is one that is in a direction contrary to the course of the usual 
nerve impulse; a descending current follows the course of the nerve 
impulse. 

In regard to the modus operandi of electricity we know little be- 
yond the fact that it is excitant and stimulant. In spite of the at- 
tractiveness of the thought, it is probably not true that nerve force 



86 GENERAL CONSIDERATIONS UPON NERVOUS DISEASES 

and electric force are the same. As an irritant it is more likely that 
electricity excites, and unites with or completely annihilates nerve forces 
according to its strength, duration, etc. In this way it probably acts 
precisely as any other physical agent. In moderate dosage it is a 
stimulant tonic ; in large dosage it is a violent excitant ; in overwhelm- 
ing dosage it is a physical destroyer. In administering electricity this 
mechanical effect of it must never be lost sight of and the nature of 
the pathological condition — in a word, a correct diagnosis — must be 
established. I once saw a complete paraplegic who had been rendered 
so immediately after the second application of a strong galvanic current 
to his spine by a physician who diagnosed his trouble as rheumatism, 
though the entire history of the case for many weeks previously showed 
that a myelitis of traumatic origin was present. The patient died less 
than a year later, presenting a typical clinical picture of transverse 
dorsal myelitis. 

Only in some of the neuroses, neuralgias and diseases of the lower 
or peripheral neurones is electricity of much avail. In the neuroses 
and neuralgias all forms of electricity may be usefully employed. In 
the degenerative and trophic troubles of the lower neuro-muscular ap- 
paratus galvanism and faradism are the chief forms to be relied upon. 
Treatment should be given as a rule daily or every other day for six 
weeks or longer. In the neuroses the middle of the afternoon seems 
to be the best time. Seances, should average about thirty minutes ; 
longer under some circumstances, shorter under others. The proper 
dosage and other details of administration will be mentioned under the 
head of the particular diseases in which it is recommended. It may be 
stated here, however, that for its psychic effect and superficial influence 
the static current with its spark and other modifications is probably the 
most useful. Therefore it is to be commended in hysteria and certain 
other mild psychoses, in some neurasthenias and neuralgias. 

The galvanic current is probably the mest generally useful. It 
reaches the deeper parts, though not to the same degree as is some- 
times imagined, especially about the head and in the spinal cord, when 
employed in moderate or safe dosage. It is well to remember always 
that the anode is rather soothing in its effect, whereas the cathode is 
exciting and irritating. Only moderate and accurate!) measured cur- 
rents should ever be employed. 

The faradic current is more superficial in its influence and is 
generally useful in peripheral nerve and muscular troubles. There is 
no great difference between the effects of the electrodes, but the sec- 
ondary current is stronger and more irritating than the primary. The 
dosage of the faradic current is usually regulated by the sensations of 
the patient and the amount of muscular contraction. Dana tabulates 
the special methods of applying the galvanic and faradic currents thus : 

1. General galvanization and faradization or general electriza- 
tion. 

2. Local electrization by galvanization of the brain, of the neck. 
of the spine, of the special senses, limbs and viscera. Or by faradiza- 
tion of the neck, spine, limbs and viscera. 

3. The combined faradic and galvanic currents. These are given 



GENERAL CONSIDERATIONS UPON NERVOUS DISEASES 87 

by means of the De YVatteville switch. General and local electrization 
can be given in this way. 

4. The polar method. This is employed chiefly in using the gal- 
vanic current. The indifferent electrode is placed on the sternum or 
back and the other electrode applied wherever indicated. 

5. Cataphoric electrization by means of Peterson's electrode. 

6. Electrolytic applications are used in enlarging strictures and 
affecting inflammatory deposits and neoplasms. 

Electro-diagnosis is referred to in the chapter on symptomatology 
and the examination of the patient. 

The factors that enter into elimatotherapy are largely physical in 
character and involve barometric pressure, purity of air, temperature, 
moisture, sunlight, wind, social and endemic conditions. As a rule 
nervous troubles are not much directly affected by these conditions, 
though the underlying diatheses upon which they depend may be very 
greatly so. In a general way neurasthenics prefer a warm, marine 
climate. Sea voyages are good for them, particularly on account of 
the enforced rest of mind and body that they involve. If stimulation 
is needed, high, rarified inland climates are to be recommended. Health 
resorts, such as those of Colorado and southern California, the West 
Indies, the Riviera and central Germany, are popular, but a new and 
virgin soil is sometimes better, away from the sight and thought of 
the presence of other invalids. A wild ranch life, a roughing of it in 
the forests of Canada, even a year or more on a good Mississippi Valley 
farm, is to be preferred to any popular resort, with its crowded cara- 
vansaries, its social competitions and its gaudy and shallow artificiali- 
ties. What a neurasthenic generally needs above all else is radical 
change of environment and of thought with rest. This is hard to ob- 
tain at the established resorts. 

Little need be said here in regard to the medicinal treatment oi" 
diseases of the nervous system. Except for the control of symptoms. 
medicines play but a minor role. Infections and underlying diatheses, 
such as tuberculosis, syphilis, gout, rheumatism and malaria, call for 
their special medication. So do anaemia and other blood conditions. 
The laity have not yet learned, and some physicians ajso, how little 
medicine does in some diseases; for on goes the expenditure of money 
and the swallowing of all sorts of patent nostrums, in spite of the fact 
that the pathological conditions show the utter uselessness of it. A 
badly disciplined girl is plied with valerian and asafcetida ; an ad- 
vanced tabetic takes hundreds of pills of so-called alterative.^ : and 
hemiplegics go on begging for some magic elixir which will relieve 
them of their imperfect speech. It is astonishing what crudity of 
ideas and credulity of belief are exhibited thus in connection with dis- 
eases of the nervous apparatus. A man is reconciled to an amputated 
limb, but for a lost memory he hunts the world up and down for a 
restorative. When he is told by competent authority that he has an 
incurable valvular heart lesion he seeks for relief, but not cure: when 
equal authority tells him he has an incurable optic atrophy, ho offers 
a million dollars for a remedy and consults with the m rant 

and superstitious. 



88 GENERAL CONSIDERATIONS UPON NERVOUS DISEASES 

In no class of diseases is the doctrine of laissez-faire and the maxim 
of nil nocere more to be remembered than in those of the nervous sys- 
tem. There is always less danger in doing too little than in doing too 
much. The power of self-restraint and the maintenance of a masterly 
inactivity should be learned by the physician here if anywhere at all. 
If patients are clamorous, as they usually are, that something should 
be done, be honest with them, or at least with their family, and state 
the utter uselessness of treatment if it is useless. One's reputation is 
thus guarded and his conscience put at ease. If still the patient de- 
mands something,, inform the family that you will prescribe a placebo 
for its psychic effect. Everybody will be happy then, so far as hap- 
piness can be attained under the circumstances. 

Under no circumstances carry on a deception with yourself on 
the one side as the deceiver and the patient and all his family on the 
other as the deceived. Let the burden be shared partly by the family. 
It is legitimate to proceed in this way often to keep a foolish and self- 
willed individual from the hands of ignorant, greedy and unscrupulous 
quacks, both medical and religious. 

Serum Therapy and organotherapy seem to have a limited field 
of usefulness in neurology. They are still, however, in the experi- 
mental stage; except perhaps the use of the thyroid gland and its ex- 
tract in cretinism and myxcedema, where organotherapy has afforded 
most brilliant results. 



SECTION B. 

THE NEURONIC DISEASES. 

Parenchymatous Functional and Degenerative Troubles. 



THE NEURONE AND THE NEURONIC STRUCTURE OF THE 
NERVOUS SYSTEM. 

I have already referred to the fact that the nervous system, as it 
is known in general anatomy, is a large, complex, compound organ 
with a more or less uniform structure and function throughout all of 
its parts, but with an apparent difference of function in different parts 
on account of the different sorts of end-organs and tissues with which 
those parts are respectively connected. Viewed thus as a single organ, 
we find the nervous system composed everywhere of three distinct sets 
of histological elements dividing between them two important func- 
tions. 

The exhibition of nerve force is the specific function of the nerve- 
cells which with their processes are now called neurones. The nour- 
ishment and support of these nerve-cells, and the holding of them to- 
gether in ganglionic masses, constitute the specific function of the 
neurogliar and connective tissue, blood-vessels, lymphatics and epithe- 
lium. 

The former are the real functionating parts of the nervous system 
and so far are to be regarded as the neural tissues. The latter does 
not functionate in any specific way and accordingly may be looked upon 
as a non-neural tissue. 

Neuroglia is not found outside of the nervous system and will 
therefore need a little further explanation after I have considered the 
nerve-cells. 

The connective-tissue, blood-vessels, lymphatics and epithelium 
do not differ from the same elements in other parts of the body and 
hence need no further description here. The various end-organs and 
tissues with which the nerve-cells are in communication, and through 
which they reveal their activities, are included in the descriptions of 
the skin, the muscles, the organs of special sense, etc., in works upon 
general anatomy and histology. 

The Neurone and Neurone Doctrine. 
( )f all the generalizations of science none have been more brilliant. 
more illuminating, more practical than the Neurone Doctrine. Like 



90 THE NEURONIC DISEASES 

all these great scientific generalizations, as for instance, the law of 
gravitation, the atomic theory of chemistry, evolution, the nebular 
hypothesis and the undulatory theory of light, it is an inference merely, 
drawn from and propounded to harmonize a great mass of seemingly 
anomalous and unrelated facts and phenomena. It is not put forth as 
an infallible truth. It is open to future modification, and if need be 
to entire annihilation, should future discoveries be made that contra- 
dict its present teachings. 

Science, to be worthy of the name, must be something more than 
a catalogue of disjointed observations. If it hopes to escape chaos, or 
to make real progress, it must have a working basis, a theory, a plan, 
a rational and well-founded idea whereon to advance. Such is the 
neurone concept first clearly stated by Waldeyer, of Berlin, in 1891, 
and modified and elaborated by the work of Golgi, Raymon y Cajal, 
Van Gehuchten, Schafer, Sherrington, Bethe, Apathy, Batton, Held, 
Hodge, Vas, Barker and others. 

The special value of the doctrine lies in the fact that it puts many 
hitherto unexplained phenomena in the nervous system upon a satis- 
factory anatomical basis ; and it enables one to comprehend and to 
teach better than has hitherto been possible, the various nervous pro- 
cesses whether physiological, pathological or psychological. 

Neurosis and psychosis, organic and functional, inflammatory and 
degenerative, are some of the terms, bandied about in neurological 
pathology that indicate the unsettled state of much of our knowledge 
even to-day of the real nature of neurological processes. Like a 
mariner without a compass, we have been buffeted about upon the 
parenchymatous and interstitial, the nuclear and protoplasmic, the 
fibrous and cellular, the vasomotor and molecular waves until we have 
almost despaired of ever reaching terra Urma. The simultaneous ap- 
pearance of peripheral and central manifestations in tabes, the galvano- 
faradic dissimilarities between the central and peripheral palsies, the 
very raison-d' etre of the so-called systemic and non-systemic diseases 
have hitherto received but scant explanation. And as far as the pathol- 
ogy of the bcte-noire of medicine, hysteria, the imagination has toyed 
in our ignorance riotously with it or in hopeless despair left it severely 
alone. 

The neurone theory, with all its imperfections and unanswered 
questions, and founded as it is upon a limited number of facts, sends 
a brilliant ray of light into this mass of darkness and promises con- 
gruity where all has been incongruous. The following statements in 
connection with the theory seem to be warrantable at the present time : 

a. The nervous system is not a uniformly continuous, united 
entity, but is made up of a mass of distinct and disconnected nervous 
units. Discontinuity is the rule. 

b. These nervous units (neurones), each consisting of a cell- 
body with processes, have taken the place of the cells and fibres of the 
older histology. 

c. No cell-body is connected with any other cell-body : nor do its 
processes anastomose with those of its neighbors. 

d. The terminal processes of neighboring neurones intermingle 



THE NEURONIC DISEASES C)[ 

without anastomosing. Sometimes the terminal branches of the pro- 
cesses of one neurone surround and immesh, as in a net, the body of a 
neighboring neurone. This is spoken of as an arborization, a teloden- 
<irion, or a synapse. 

e. The cell-body is for the nutrition of the neurone while its pro- 
cesses are for the transmission of nervous impulses. 

The following deductions form parts of the theory, but as yet have 
not been completely established : 

a. In some instances, minute neurofibrils may anastomose and 
connect directly sensory with motor, and motor with sensory elements. 

b. Xerve force or nervous excitability is a quality of the entire 
neurone (cell-body with its processes) and is not merely a force evolved 
by the cells alone and then sent out along various nerve fibres. 

c. Afferent and efferent are relative terms, since strictly speaking 
there are no currents in the neurones, but merely states of excitability. 

d. Neurones are sensory or motor in function, solely according 
to the nature of the end-organs with which they are respectively con- 
nected. 

e. Nervous excitability or nervous impulse is in all probability 
a molecular force, involving changes within the substance of the neu- 
rone. 

f. The neurones, or at least their terminal processes, are en- 
dowed with a low grade of amoeboid movement. This is very ques- 
tionable. 

g. By means of this amoeboid (expansion and contraction) move- 
ment, the terminations of neighboring processes are made to approxi- 
mate and separate from one another. This enables one neurone to 
•excite or transmit its own excitability to the neighboring neurones. 
This is extremely doubtful. 

h. In some instances, this nervous excitability may be transmit- 
ted from one process to a neighboring process by means of the inter- 
vening neurogliar elements which are derived from the same blasto- 
dermic layer as the neurones themselves are. 

The Neurone. The neurone or nerve-unit consists of a nucleated 
cell-body with a dozen or more processes. These processes are not 
nerve fibres, but extensions from the cell-body. One, or at most two, 
of them are very long and are called neuraxoiics; the others are short and 
are named protoplasmic processes or dendrites. A neuraxone consists 
of an axis-cylinder surrounded by a medullary substance. Outside oi the 
central nervous system, the medullary substance is again surrounded 
by a nucleated covering known as the neurilemma. Each axis-cylinder 
is composed of a number of primitive fibrils, held together by a kind of 
cement-like substance. Obersteiner has counted as many as fifty fibrils 
in one axis-cylinder of the sciatic nerve of a frog. It is readily under- 
stood, therefore, how the distal ends of the neuraxoneS may split up 
into numerous brush-like branches (arborization), and how along their 
course they may give off at right angles short lateral branches (col- 
laterals), which also terminate in an arborization. These primitive 
fibrils of the axis-cylinder, when traced backward into the cell-body, 
are seen to pass without interruption through the cell-substance, or 



92 



THE NEURONIC DISEASES 



FIGURE 17. 




Diagram of a lower motor neurone. (After Barker.) D, a motor cell from 
anterior horn of the cord with its protoplasmic processes. Ax, axis-cylinder 
process. S F, collaterals. M, medullary sheath. N R, node of Ranvier. N of 
N, nucleus of neurilemma. Tel, the ending in striped muscle-fibre, M'. N, the 
nucleus, and N' nucleolus of the cell-body. 



THE NEURONIC DISEASES 



93 



to bend within the cell-body and terminate in one or more of the short 
processes or dendrites. On the other hand, the fibrils of the dendrites 
do not all pass into the neuraxone but some of them cross through the 
cell-body and continue on into the other dendrites. 

The cell-body itself, sometimes called the perikaryon, consists "of 
a mass of protoplasm inclosing a nucleus and a nucleolus. It measures 
from 1-3500 to 1-250 of an inch in diameter. Its contents are com- 
posed of a semifluid albuminous substance, like the white of an egg. 
and is spoken of as the protoplasm or cytoplasm. Within this cyto- 
plasm lies the nucleus, inclosing the nucleolus. The cell-body proper 
is a network of granular fibres, between which is the yiscid fluid called 
the paraplasm. In this network are the chromophyllic granules of 

FIGURE 18. 




Golgi cell of Type I. From the optic tract of a cat. The axis-cylinder or 
neuraxone is only moderately branched, giving off collaterals at points marked c. 
The dendrites are numerous and abundantly branched. (After Kolliker. ) 

Nissl which stain deeply with aniline dyes. Xot all cells possess these 
granules. Those that do not are called somatochromes, while the others 
are named karyochromes. These granules are thought to contain the 
nutrient substance of the cell-body, while its functional activity is sup- 
posed to depend upon the paraplasm. A trace of pigment is usually a 
■constituent of the cell-body. 

The nucleus and nucleolus are both likewise reticulated and stain 
deeply. Such in brief is the minute anatomy of a neurone, the ultimate 
unit of the functionating or excitable part of the nervous system. 

There are three typo of neurones, which differ, however, more 
in degree than in kind. The) are the motor, the sensory and the sym- 
pathetic. 

The motor is the simplest. An example of it may be seen in the 
cell-body found imbedded in the anterior horn of the spinal cord, with 
its dozen or more dendrites extending for a short distance in all direc- 
tions, eyen into the posterior horn, and its single, long neuraxone 1 
ing out through the anterior root to its termination in some distant 
muscle-plate or motor end-organ. 



94 THE NEURONIC DISEASES 

The sensory neurone is somewhat more complex. It may be seen 
with its cell-body resting midway in its make-up in the ganglion of 
the posterior spinal root and its two processes extending in opposite 
directions, one going out to the skin or distant special end-organ of 
sense, and the other passing up through the posterior root into the 
cord as far even as the medulla oblongata. This neurone is sometimes 
described as though its neuraxone were bifurcated shortly after it had 
left the cell-body and the two branches, T-like, were directed in oppo- 
site ways. It is better, however, to regard the central process as the 
neuraxone and the peripheral process as a modified dendrite. 

The sympathetic neurone partakes of the nature of both of those 
just described, but its neuraxone is non-medullated. 

. FIGURE 19. 




Golgi cell of Type II. From the cerebrum of a cat. (a) Axis-cylinder is very 
much branched. The dendrites are coarse and are covered with "thorns" or 
"gemmules." (From Kol'iker.) 

The accompanying illustrations will show some other character- 
istics and other subsidiary types of neurones. Note the enormous num- 
ber of dendrites in the Golgi cell of this author's type I and the pecu- 
liar "thorns or ''gemmules' 7 on some of them in his type II. Observe 
the enormously complex arborization of the Purkinje cell process illus- 
trated by Van Gehuchten. 

In regard to the physiology of the neurone, the experiments of 
Hodge, Nissl, Vas, Mann, and others are fascinating i n the extreme. 
The movements of the so-called chromatiri-bodies and of the peculiar 
dumb-bell-shaped objects in the midst of the mass of crossing and re- 
crossing fibres within the cell have been distinctly observed and por- 
trayed. Nissl even goes so far as to assert that the arrangement and 
movements of these intracellular fibrils and chromatin-bodies enable us 
to distinguish motor from sensory cells. His views in this respect, 



THE NEURONIC DISEASES 95 

however, have not been universally accepted. The activity of the neu- 
rone results in a diminution in the size of its cell-body, a lessened 
power for absorbing stains ( diminished power of assimilation ) , vario- 
lation (the using up of its own substance) and a marked alteration in 
the contour of the nucleus from a smooth and round to an irregular 
and jagged edge. Gentle stimulation of the cell*causes it to swell and 
the chromatin bodies to move towards its periphery. Overstimulation 
results in a shriveling up of the cell and a complete or almost com- 
plete disappearance of the chomatin bodies. The dumb-bell bodies, 
under the same conditions, stain more deeply and do not disappear. 
Mere activity, over-exhaustion, poisoning from retained excrementi- 
tious products (auto-intoxication) or from toxins introduced from 
without, such as alcohol, absinthe and nicotine will all provoke the 
same histological changes in the neurone. Rest restores its normal ap- 
pearance, but only after a considerable lapse of time. This goes a long 
way to prove that the main function of the cell-body is the nutrition of 

FIGURE 20. 




A Purkinje cell of the cerebellum, illustrating a marvellously complex abori- 
zation of a single neuraxone pr. cyl. (After Van Gehuchten.) 

the entire neurone. It likewise is not a little suggestive of the true 
nature of many of the nervous diseases, of the cause of many of their 
peculiar manifestations, and the direction in which a restoration of the 
integrity of the nervous apparatus is to be looked for. 

The neurones are developed from {he neuroblasts of the embryo, 
which in turn are evolved from the epiblastic layer of the developing 
>vum. The figure after J. Kollmann shows admirably the different 
stages of the development of the neurones. 

The neuroglia consists of a peculiar variety of cells which 
found only in the nervous system and which, are developed from the 
spongioblasts of the embryo. These cells seem to have no other fuirc- 



9 6 



THE NEURONIC DISEASES 



tion than to form a supporting network, scaffolding as it were, for the 
neurones. Until quite recently the neuroglia was spoken of as a 
variety of connective tissue. It is unlike the latter, however, in be- 
ing developed from the epiblastic instead of the mesoblastic layer of 
the growing ovum, and in containing the peculiar chemical substance 
neurokeratin, which % a variety of the keratin seen in the hair, nails 
and epidermis. 

The neurogliar cells are sometimes called "spider cells'' because 
of the relatively small size of the body and the very numerous and 

FIGURE 21. 




Axones of {mo- 
1 tor) ventrul 
root. 



Medullary tube 



Neuroblast. 



Transverse section of the spinal cord of the chick to show the neurones in 
the different stages of development. Right side is from a five day chick ; the 
left side from a two day chick. (After Kollmann.) 

highly ramified processes. The body is varied in size but is more or 
less round in shape. It consists of granular protoplasm in which is 
imbedded a large nucleus with a nucleolus. So fine and numerous are 
the processes, that where the neuroglia is found in abundance, as for 
instance, around the central canal of the spinal cord, in the periphery 
of the cord, beneath the ependyma of the ventricles of the brain and 
below the pia mater, the tissue resembles almost a homogeneous matrix. 
According to Weigert the processes stain differently from the cell- 
body and thus would seem to have a different composition both chem- 
ically and physically. In states of inflammation the neurogliar cells 
are seen to swell up and serve as scavenger cells in carrying off noxious 
products. 

The Neuronic Architecture of tlie Nervous System. 

Having now studied the elements that enter into the composition 
of the nervous system and learning that the functionating neurones, 
according to Donaldson, make up fifty-three per cent, of its bulk (at 
least in the brain and spinal cord), while forty-seven per cent, con- 
sists of the sustentacular tissue (neuroglia and connective tissue net- 



THE NEURONIC DISEASES 



97 



work), it remains to be seen how these elements are arranged in rela- 
tion to one another in the architecture of the sum total or completed 
apparatus. 

Imbedded in the sustentacular tissue everywhere are the innu- 
merable neurones. Each neurone constitutes a unit in itself, so that 
it is quite improper to speak of nerve-cells and nerve-fibres as distinct 
and separate structures. 

The aggregate of all these countless neurones constitutes the real 
functionating nervous apparatus and their disease alone constitutes 
real inherent nervous disease. They are not scattered promiscuously, 
however, throughout the meshwork of supporting tissue but are more 
or less regularly grouped and arranged, both in relation to particular 
parts of the body and in relation to one another. 



FIGURE 22. 




Glia cells from the cerebral cortex of a rabbit. (After Benda.) 



Upon this grouping we have established certain artificial gross 
anatomical divisions of the nervous system, such as the brain, the spinal 
cord, the peripheral nerves and the sympathetic system. These divis- 
ions, however, are arbitrary, for the neurones which we find in them 
are always the same in all essentials. 

Somewhat more significant than these gross anatomical sub- 
divisions of the nervous system, is its obvious arrangement into masses 
of gray and white matter. A close examination of this reveals the fact 
that what is called gray matter is only the anatomical bunching together 
of the bodies of the neurones, while the white matter represents the 
assemblage in close proximity of their neuraxones. in the sympa- 
thetic ganglia, in the ganglia on the posterior spinal nerve roots, in the 
gray matter of the central cord, in the ganglia and nuclei of the cranial 
nerves, in the optic thalami and corpora striata, in the cortex, and in 
fact wherever this so-called gray matter is found, there are congre- 
gated in close quarters the bodies of the neurones. In the spinal 
nerves, in the white columns of the cord, in the centrum ovale of 
the brain, and wherever else so-called white matter is observed, there 



9& THE NEURONIC DISEASES 

run the neuraxones extending out from the cell-bodies of the neu- 
rones. It is obvious, therefore, that there is no very great signifi- 
cance to be attached to this subdivision of the nervous tissue, namely, 
into gray and white matter. 

It is clear that the anatomical and functional relationship of the 
individual neurones themselves to one another is the great and im- 
portant underlying fact in the structure and specific activity of the 
nervous system. There is no single neurone anywhere in the body 
whose extent, with the aid of its neuraxone and dendrites, is so enor- 
mous that it can reach from one extreme end of the nervous system 
to the other. And yet we know that both afferent and efferent im- 
pulses traverse the entire length and breadth of the body. They must 
clearly, therefore, pass over several successive neurones in their long 
journeys. There is an end-to-end arrangement of the neurones of the 
various functional pathways along which the impulses travel between 
center and periphery. It is necessary to be familiar with the construc- 
tion of these afferent and efferent pathways, to know just where and 
how their constituent neurones begin and terminate, and to comprehend 
what functional relationship one neurone bears to its neighbor when 
both are constituents of the same direct and single pathway. 

In an earlier paragraph I described three typical forms of neu- 
rones and showed that whereas their differences were not essentially 
important, they subserved respectively, motor, sensory and sympathetic 
functions. Other types of neurones might have been described, espe- 
cially in the cortex, the commissural, and the association tracts of 
the brain. In all essentials, however, they are practically the same. 
If I describe the afferent and efferent projection paths upon the basis 
of their neuronic constituents, it will suffice to indicate the general 
neuronic architecture of the entire nervous system. The principle 
underlying it will have been portrayed. Future discoveries may en- 
large our ideas but it hardly seems probable that any very great alter- 
ation in the general principle of construction will ever hereafter be 
made. 

The entire length of the pathway for all motor impulses from 
brain to muscle seems to be made up of two long neurones, placed 
end-to-end. Of course it must be understood that the aggregate motor 
tracts are constituted of a great number of neurones lying side by side. 
Longitudinally considered, however, each individual outgoing impulse 
must, after it leaves the brain, traverse two neurones before it ex- 
pends itself upon the appropriate muscle. The first or central neurone 
has its body imbedded in the cortex near the fissure of Rolando and 
projects its neuraxone down through the cerebral crura and the pyra- 
midal tracts of the cord, to its termination in an arborization around 
some cells in the cranial nuclei of the medulla or in the anterior horns 
of the cord. The second or peripheral neurone has its body nestling 
in a cranial nucleus or anterior horn and extends its neuraxone out 
through the nerve to the end-plate of the muscle it is created to sub- 
serve. 

The two sections of this pathway may well be named cortico-spinal 



THE NEURONIC DISEASES 



99 



and spino-muscular respectively. The central neurone inhibits, stimu- 
lates, controls and regulates the action of the peripheral neurone. It 
moreover assists in maintaining its nutrition. The peripheral neurone 
on the other hand stimulates the contractions of the muscle and pre- 
sides over its nutrition. 



FIGURE 23. 



A.C.N 




Multipoint 

Cello/ Ant 

Horn 



Schema of the relationship of the neurones in the sensory and motor path- 
ways between the brain and the periphery. (After Halliburton and Mott.) 

The pathway for the afferent or sensory impulses is more com- 
plex and as a rule is made up of a number of end-to-end neurones. 
i ne outermost or peripheral neurone has its body hidden away in the 
ganglion on the posterior spinal nerve-root. As a modified dendrite 

one of its processes extends outward in the nerve to the skin, or some 
special end -organ, while the neuraxone passes inward and upward to 



LolC. 



IOO THE NEURONIC DISEASES 

the spinal cord to terminate in an arborization around the cells at 
the top of the column of Burdach and Goll. These ceils constitute the 
bodies of the next succeeding neurones whose neuraxones again pass 
upward to terminate in an arborization around the cells found lying in 
the optic thalamus. These cells once more extend their neuraxones up- 
ward to terminate and arborize around the cell-bodies of other neurones 
imbedded in the cerebral cortex. 

There are great variations in the neuronic arrangement of the 
sensory paths. They will be discussed somewhat more in detail when 
the anatomy and physiology of the brain and spinal cord are taken 
up. Here I merely wish to call attention to the fact that the afferent 
and efferent paths between the brain and the periphery are formed 
of a series of neurones placed end-to-end, that make the progress of 
the impulse a step-like one. There are special neurones and neuronic 
paths that do not emerge from the central nervous system at all but 
serve to connect different parts of it together and to approximate the 
inner ends of the various projection paths. In fact we are only on 
the threshold of knowledge in regard to the bewildering interlacement 
of all these countless neurones. It is hardly probable that what we 
denominate commissural, associative and projection tracts contain 
all of the neurones that it is possible for us to know later. Indeed we 
have still a goodly amount to learn in regard to these even, and the 
future will doubtless reveal to us greater complexities in the innumer- 
able pathways by which impulses travel hither and yon and in and out of 
the nervous system. When we will have learned more of these pathways, 
we will doubtless be able to understand some diseases that are now un- 
explainable. Already we are sufficiently acquainted with some of them 
to enable us to classify some organic and functional troubles in accord- 
ance with their location. 

There are some diseases that seem to have their seat entirely 
within the neurones. Pathologically and symptomatically they are, in 
the literal sense of the word, nervous diseases. The surrounding tis- 
sues may not be affected at all in them or only secondarily so later on. 
Etiologically, heredity, toxaemic and general cachectic states play the 
most important role in their development. Sometimes the heredity 
is direct, at other times it is indirect. The inheritance may range all 
the way from a mere neuropathic tendency to an actual and gross de- 
fect. So influential are the inherited and congenital conditions in the 
development of these diseases that it is doubted by some whether with- 
out such a neuropathic predisposition these diseases would ever appear 
as a result of the exciting causes usually given for their appearance. 
It is not believed by many that mere strain, exposure, overexertion, 
intoxication or infection would ever induce a pure neuronic disease if 
the neurones themselves were not previously predisposed by an inher- 
ited weakness. It is contended that such active causes would produce 
in those who were endowed with a vigorous heredity, diseases of the 
other tissues also, such as hemorrhage and inflammation. 

We divide these diseases nevertheless into the inherited and the 
acquired. This is a convenient division for practical purposes but it 



THE NEURONIC DISEASES IOI 

is about as strictly scientific and logical, in view of what we already 
know, as would be their division into organic and functional. 

All diseases in their last analysis must logically be assumed to be 
organic. A change of function to that which is non-function presup- 
poses by all the laws of reason, a change m the functionating substance. 

Organic and functional are relative terms to indicate the efficiency 
and inefficiency of our present means of investigation. The pains of 
tabes differ only in degree, and sometimes not at all, from the pains of 
idiopathic neuraglia, and yet merely because we can see the degen- 
erated conditions in the former we speak of it as an organic disease, 
while the unseen changes in the latter we denominate functional. 

Pathologically there is in all probability a mere difference of de- 
gree rather than of kind between the so-called organic and functional 
neuronic diseases. A neurosis is a degenerative trouble as truly as 
is a wasted condition of the neurones in some form of systemic disease. 
It may be a more widely diffused or a lesser degree of degeneration, 
but that it is a condition of functional and therefore inherent, degen- 
eracy can not be reasonably gainsaid. To conform with popular usage, 
however, particularly as we are in need of many data to make our con- 
tention absolutely undeniable, I will continue to divide the neuronic 
affections into the organic and functional. As some of the former con- 
fine themselves to, or at least begin in, a particular set of neurones, they 
may be further subdivided. In a gross way the same is true of the 
neuroses. 

The following seems to me to be a warrantable classification of the 
pure neuronic diseases: 

The Functional Neuronic Diseases. 

(Neuroses and Psychoneuroses.) 
i. Those of the Cerebrospinal System. 
2. Those of the Sympathetic System. 

The Organic Neuronic Diseases. 

(System Diseases.) 
i. Those of the Afferent System. 

2. Those of the Efferent System. 

3. Those of the Afferent and Efferent Systems. 

FUNCTIONAL NEURONIC DISEASES. 

THE NEUROSES. 

All disease must be functional in its incipience. Some dis< 
remain functional; others go on to cause slight or minute changes un~ 
discoverable by our present means of investigation; while still others 
advance to the production of gross microscopic and macroscopic altera- 
tions, much destruction, and even annihilation of tissue. The latter 
changes we can see and so we call them Organic ; the former we cannot 
see, and so we still must denominate them Functional. 

This use of the term functional has cine to be specific. We do 
not include the gross organic diseases in the class of functional trouble-. 



102 THE NEURONIC DISK ASKS 

though as a matter of fact they involve even greater functional dis- 
turbances than do the latter. 

The specifically called functional diseases are sometimes denomi- 
nated the Neuroses. As these diseases are, so far as we can deter- 
mine, the result of hereditary, nutritional, hygienic and general toxaemic 
influences, they implicate all of the neurones. They are diseases, 
therefore, of the nervous apparatus more or less in toto, and from their 
inherent nature are the most specific of all those of the nervous system. 
They are diffuse affections within the neuronic network. They there- 
fore are sometimes called the Psychoneuroses. They do not all present, 
for some reason unknown to us, exactly the same degree of vividness 
in their mental, sensory and motor manifestations. Some of them, like 
hysteria, take on a psychic complexion ; others, like hemicrania, lead 
with sensory phenomena ; still others, like the myospasms, seem almost 
to be entirely motor. 

The characteristic of these neuroses or psychoneuroses is that 
they all present a clinical picture in which all forms of nervous symp- 
toms appear, though not in all patients nor in all periods of the disease. 
Their diffuse localization is well represented in the name psycho- 
neuroses. 

The hereditary psychoneuroses are of the nature of biological 
defects. They are instances of racial or familial degeneracy. They 
bespeak a functional inadequacy in the neurones as a result of an 
embryological degenerative inferiority in their structure. As diseases 
they are therefore not hopeful from the standpoint of prognosis or 
therapy. 

The congenital psychoneuroses are hardly much more favorable. 

The acquired psychoneuroses are somewhat more encouraging, 
though as some heredity, less in intensity perhaps, plays a role in their 
evolution, they are at times obstinate and need both judicious and 
decisive management. Their prognosis under given conditions is ex- 
ceedingly bright. 

We can conveniently divide the psychoneuroses into those whose 
symptoms point most prominently to the cerebrospinal apparatus on the 
one hand, or to the sympathetic system on the other. The functions 
of the latter are so markedly distinctive that when they are deranged 
we sometimes refer to them as angioneuroses or trophoneuroses. It 
goes without saying, of course, that this classification is liable to modi- 
fication under the development of future knowledge. 

A. THE CEREBROSPINAL NEUROSES. PSYCHONEUROSES. 

HYSTERIA. 

Hysteria is recognized at the present day as a mental trouble, 
which, unlike the forms of psychosis usually classified under the old 
term insanity, reveals itself more distinctively through the motor, 
sensory and trophic apparatuses than they dc. The paralyses, anaesthe- 
sias and other stigmata of the disease are clearly mental in origin. 
Moreover, the disturbances of the memory, volition and intellect , cans- 



THE NEURONIC DISEASES IO3 

ing a greater or less transformation of the patient's personality, the 
ego, indicate the psychic nature of the disease. 

The resemblance of many of the phenomena allied to hysteria, 
such as the histrionic manifestations, the mimicries, the hypnoses, the 
catalepsies, the somnambulistic actions, as well as the character of the 
typical hysterical symptoms themselves, have inclined most authors to 
regard the trouble as largely a disturbance of the higher psychic or 
cortical inhibition, with a relaxation of the lower or subcortical, or 
ganglionic activities. It is assumed that there are, so to speak, two 
minds, the conscious and the subconscious, the seat of whose activity 
is not known positively, though the former is supposed to be dependent 
chiefly upon the cortex and the latter upon the lower layers of the 
cortex or basal ganglia. 

Janet speaks of hysteria as being the result of a "contraction of 
the consciousness." From this point of view hysteria may be not 
inaptly compared to the well-known spastic paralyses of organic cerebral 
disease; only in hysteria the failure of inhibition from above and the 
spasticity from below are entirely and completely in the mental or 
psychic sphere and not in the organic. While admitting that much of 
this is purely theoretical, the theory explains and covers a larger 
amount of hysterical phenomena than any explanation hitherto ad- 
vanced. 

Etiology. — The first thing that must be observed under the head 
of the etiology of hysteria is that most of the causes assign to oy the 
older writers are no longer regarded as such. The uterus, on account 
of which the disease received its name, is not the cause: nor are any 
of the sexual organs, or the sex of the individual. Not upon any single 
organ or tissue of the body can the blame be laid for the hysterical 
condition, though upon one or all of them may depend the outbreak 
of an attack. The primary cause of hysteria is to be found in the 
patient's mental make-up, his temperament, his mental instability, 
which is more or less congenital and constitutional. The secondary 
causes that may precipitate an attack of hysteria or arouse the latent 
temperament into a more or less continuous objective reality are in- 
numerable and include such factors as early education, discipline, en- 
vironment, physical abnormalities and local diseases. 

From what has just been said, ir will be readily surmised that 
heredity plays the greatest role among the predisposing causes of hys- 
teria. The heredity is usually direct and transmitted through the 
maternal ancestry. The mother, or grandmother, or maternal aunts 
of the patient will be found to have been hysterical. Frankly admitting 
the force of suggestion and close companionship between mother and 
child in the development of hysteria in the latter, it is nevertheless true 
that the hysterical predisposition is chiefly pre-natal in origin. The 
heredity is not always direct and occasionally it is transmitted by the 
father. Chorea, epilepsy, extreme neurasthenia or mental disease may 
have been the trouble in the ancestry. Chronic alcoholism, excessive 
use of tobacco and dissipation involving nervous strain may transmit to 
the offspring the neuropathic temperament that needs but an exciting 
cause to provoke a genuine attack of hysteria. 



104 T HE NEURONIC DISEASES 

Next to heredity the great predisposing cause is a false early edu- 
cation. The child being more or less neuropathic, its irritability, over- 
sensitiveness, flashes of what seem like mental brilliancy, high emo- 
tionalism and general abnormality are fondly mistaken by parents for 
evidences of exceptional talent or even genius. It is pampered and 
coddled, all its whims are humored, its doings and sayings are lauded, 
and all systematic discipline and irksome routine are completely omit- 
ted. The child becomes egoistic and tyrannous ; it loses all idea of the 
proper relationship it should bear to society ; it feels aggrieved at every 
little opposition it meets ; and as a result it grows into adult age com- 
pletely unfitted to meet the disappointments, discouragements and trials 
of life. This provokes a spirit of revolt and a tendency to be moody 
and unsocial. It may break into a violent and emotional excitation. 

For a long time it was believed that hysteria was a disease of 
women only. This was the result largely of locating the cause of the 
trouble in the uterus. The same symptoms in men were not deemed 
hysterical. Since we have given up this old pathology and pathogenetic 
explanation of the symptoms, more care has been taken in studying 
and comparing them and as a result we find that hysteria is a disease 
of both sexes and of all ages. 

The trouble appears more frequently among women than among 
men in the proportion of about ten or six to one, not because of their 
sexual but because of their nervous and mental differences. Woman's 
nervous system is more mobile and less inhibited normally than is 
man's. Some of the most typical cases of hysteria that I have seen have 
occurred in men. 

The dependence of the disease upon nervous instability is further 
emphasized by the fact that it so frequently breaks out in its most 
violent forms about the time of puberty, and from this period up to the 
thirtieth or fortieth year. Many of the neurotic symptoms of the 
climacteric are hysterical. 

It occurs in childhood and has been seen as early as two years of 
age. Passionate outbursts of temper and such manifestations as chorea 
and certain subjective sensory phenomena in childhood are occasionally 
hysterical in character. 

Hysteria is rare after the climacteric and in old age, though some 
authors speak of a senile hysteria. 

Certain races and nations seem to be more prone to the disease 
than others. It is very common among the Latin races, especially the 
French, from whom we have learned most about it. The Jews are 
very liable to it and it has been observed among certain barbarian tribes. 
The Anglo-Saxon is probably the least subject to it among the civilize 1 
races. 

There are certain exciting causes that may arouse a latent hysteria. 
Foremost among them are emotional shocks and strains, such as terror, 
anxiety, disappointed love or what may be termed psychic traumata of 
every sort. The symptoms following lightning stroke, earthquakes, 
railroad accidents and collisions are often purely hysterical. 

Sudden irritative and imitative impulses may excite a hysteric 
outbreak. This occurs in epidemics and among masses of people. The 



THE NEURONIC DISEASES 105 

mediaeval semi-religious pilgrimages, dances, the New England witch- 
craft, modern revivals, stampedes, religio-medical followings of quack- 
ery and peculiar beliefs of all sorts, many strange antics of the inmates 
of monasteries, convents, boarding schools and factories are all more 
or less attributable to the hysterical tendency. The history of these 
epidemics and outbreaks affords most interesting and sad reading. The 
folly and weakness of human nature is its most obtrusive lesson. 

Organic diseases and traumatic injuries may worK through the 
mind and nervous system to provoke and maintain a hysterical at- 
tack in one who is already predisposed. By themselves they are not 
causative of hysteria. This should be carefully remembered, for it 
explains how a removal of these exciting causes, by surgical or other 
means, often results in a return of the hysteria or hysterical tempera- 
ment into a latency which is too often interpreted as a cure, but which 
only awaits another powerful excitant to awaken it into activity. Just 
as hysteria is often symptomatically imitative of known forms of 
organic disease, so in those already predisposed it is etiologically imita- 
tive of them. 

Symptoms. — As Mobius well says, hysteria is a state in which 
ideas exert an influence to bring about morbid changes in the func- 
tions of the body. The ideas or mental state of the patient constitute 
the most, important symptoms therefore, and though not always the 
most obtrusive or the most easily elicited, they should in every clinical 
examination be most earnestly and persistently sought for. Certain 
facts stand out very prominently in regard to a hysteric's psychic 
condition. They are irritability and instability, abnormal emotionalism, 
altered volition and inhibition, and increased power of imagination. 
The mental power is not weakened, the memory is usually intact, and 
the will and intellect are about up to the patient's normal capacity. 
This leaves the imagination as the chief faculty at fault, and yet the 
increase in the power of the imagination is rather the result of the 
weakened power in the higher or controlling inhibition. Abnormal 
irritability with changeability of ideas, all the result of a congenital 
defect in the cortical structures underlying the function of mentaliza- 
tion and of an educational failure in the development of the associational 
paths supporting the proper concepts of life and its thousand and one 
relationships, is the hysterical mental condition. 

This abnormal irritability is both centripetal and centrifugal in its 
action. It is provoked abnormally by every slight inpouring impulse 
and it provokes abnormally every function of the body, motor, sensory 
and vasomotor. 

As Oppenheim points out, this abnormal irritability reveals itself 
in the sudden variations in disposition and in the pathological increase 
of normal actions. Laughing and crying become spasmodic. The 
transient normal inhibition produced by tear, anxiety, becomes paraly- 
sis. Indifference and insensibility from the same cause become Stupor, 
delirium and anaesthesia. Imaginary thoughts develop into hallucina- 
tions. Motor activity passes into spasms, contractures and cataleptic 
rigidity. 

This irritability and heightened influence of the mind are produced 



106 THE NEURON 1 C DISEASES 

by the most insignificant circumstances and often by no known reasons. 
It shows itself in unwarrantable outbursts of anger, joy, vexation, 
depression and terror. The memory may participate in this irritability, 
causing past events and sights to be recalled with such vividness as to 
throw the patient into a confused and dream-like state and to make it 
appear as though he were living in another world or in another period 
of time. With all this irritability there is a most obvious loss of the 
power of mental inhibition and self-control, especially over the emo- 
tions. There is not strictly any loss of volitional power, or aboulia, 
but rather perversion. When the patient declares she cannot act, she 
frequently exhibits at the same moment an astonishing power of voli- 
tion in other ways. The ideas which are passing through her mind at 
the instant have so altered her motives for action that her power of 
volition is shown not in the desired but in other and unexpected ways. 
Instead of loss of will, therefore, it is nearer the truth to speak of 
perversion of the will. There is no distinct weakening of the mental 
power, though feeble-minded people may be attacked by the disease. 
As a matter of fact, hysteria occurs more frequently among intelligent 
than among ignorant individuals, a truth which has its bearing, in the 
management of these cases, upon the relationship of the physician to 
the patient. 

The alterations of character, the oft-times senseless and, purpose- 
less acts, the prevarication, the instability and unreliability, the tout 
ensemble picture which so often arouses disgust and even anger among 
the bystanders, are not the result of mental enfeeblement, but rather of 
the abnormal irritability, rapid changeability, perverted memory and 
vivid imagination which cause a swift passage of ideas through the 
patient's mind. There is no fixity in her motives and she is the prey to 
every gust that whirls down upon her mental horizon. She acts logi- 
cally in accordance with her motives, albeit the acts themselves appear 
to be bizarre, willful and without rhyme or reason. 

To understand, therefore, the attitudes, the speeches, the sensa- 
tions, the whole outward manifestation of these patients one must 
closely recognize the state of mental irritability and then as far as 
possible trace the underlying ideas to their source. 

Hysteria being in that ill-defined borderland between sanity and 
insanity, its mental manifestations, which are always present, assume 
the most varied forms. Some hysterics are undoubtedly insane in the 
common acceptation of the term, while others are only weak and irre- 
sponsible, especially in the moral sphere, but would not be commonly 
regarded as insane. 

Hysterics exhibit the hallucinations, delusions and illusions of the 
most profound forms of mental alienation, down to mere prevarica- 
tion, secretiveness and other slight forms of moral delinquency. 

It is in the ethical and emotional spheres that hysteria indicates its 
relationship to mental troubles most distinctly. Certain mental mani- 
festations that occasionally occur with hysteria should not be looked 
upon as a part of the disease. They are mere complications; the two 
conditions are merely associated forms of disease due to the same 
cause. A melancholia, mania, paranoia will sometimes break out in 



THE NEURONIC DISEASES IOJ 

the course of hysteria and be erroneously named hysterical melan- 
cholia, hysterical mania, etc. 

The prognosis of such cases depends not upon the hysteria, but 
upon the insanity, and as a rule it is bad for recovery. A clear appre- 
ciation of this distinction will lead to better results in the management 
■of hysteria and to more prompt asylum confinement in the cases com- 
plicated by insanity. 

Other symptoms, often classified as hysterical, such as the impera- 
tive conceptions, phobias, like agoraphobia, pyrophobia, manias, like 
dipsomania, morphino-mania, kleptomania, are complications and 
should not be regarded as a part of the disease we are now referring to. 
They are expressive of a phrenasthenia and represent a mental de- 
pression, congenital or acquired. They often occur in hysteria, but 
they are not symptomatic of it. As mental troubles they may be modi- 
fied and colored by the hysteria that is present, and the association of 
the two sets of symptoms may be so close- that one may have much 
difficulty in determining which is the predominating and more im- 
portant disease. Here doubtless belongs the astasia-abasia so much 
studied in recent years by European neurologists. Standing and walk- 
ing are impossible, though there are absolutely no signs of disturbance 
of motility, of sensibility or of coordination when the patient is lying 
•down. Only when he gets up and attempts to walk docs the difficulty 
reveal itself. Moving on all fours, swimming and other forms of 
movement may still be performed. 

There are several possible explanations. It is clearly psychic in 
origin and may be a sort of specific psychic ataxia or special form of 
mental incoordination, loss of the memory pictures for walking. 

A somewhat similar condition obtains in some of the occupation 
neuroses. 

True hysteria, uncomplicated, is characterized by three particular 
forms of psychic disturbance observed mostly in paroxysms. 

The first is an indefinite sense of fear, unaccompanied by definite 
conceptions such as occur in the well-known phobias. With this sense 
of fear is a feeling of precordial oppression and cardiac palpitation. 

The second is a state of hallucinatory delirium, in which the patient 
shows the manner and fancies of one under the influence of frightful 
dreams or visions. He slinks away or strikes at the attendant. From 
this half-dreaming state a dash of cold water or other forcible form of 
stimulation may arouse him. 

The third state is that in which somnambulism, hypnotism, 
lethargy, catalepsy, etc., obtain. 

All of these three states are typically hysterical and arc dependent 
largely upon the abnormal activity of the affective faculties, the feel- 
ings, emotions and imagination. 

Next to the mental state in frequency and importance are the 
presence and the character of the sensory symptoms. Though tin— 
symptoms are subjective, like the mental., and are therefore that much 
less valuable as positive indication- of disease, they can be examined 
and tested objectively or at least made to provoke objective signs that 



ro8 



THE NEURONIC DISEASES 



FIGURE 24. 




Hysterical anaesthesia. 



THE NEURONIC DISEASES IOQ 

are most valuable in indicating not only the presence of, but the real 
nature of the trouble. 

The first great law to be remembered in regard to hysterical sen- 
sory phenomena is that they are physiologically and anatomically 
mental and not neural. They do not localize themselves in accordance 
with nerve distribution or cortical limitations ; they involve those parts 
of the body known only to the patient's ego, or his consciousness. 
They are therefore more or less co-extensive with the segments of the 
body and not with the mere cutaneous area of this or that set of nerves. 
The hand, the arm, the leg, the half of the body, the glove or stocking 
type of distribution indicate the areas affected. The special senses 
show the same peculiar mental disturbance. In hysterical blindness it 
is mental vision, not actual vision that is affected. 

A second law to be remembered in regard to these sensory phe- 
nomena is with regard to their great changeableness and instability. 
They come and go with rapidity and uncertainty. They may be mild 
or marked throughout their entire extent and continuance, or they 
may be mild in one part of the body while severe in another. One 
side may show hyperesthesia, the other anaesthesia. The visual field 
of one eye may be immensely more altered than that of the other. A 
reversal of the conditions may even take place at a most unexpected 
moment. It is this fact that renders hysterics the willing and self- 
deceived dupes of religio-medical quacks, to whom they give fulsome 
testimonials of astounding cures. 

All forms of sensation may be affected in hysteria. Smell, taste, 
hearing and sight of the special senses and tactile, temperature and pain 
of the cutaneous senses, and even the muscular sense may be altered. 
The sense disturbance itself may be exactly that of an organic disease ; 
the only way it can be determined as hysterical, mental or functional 
is by carefully considering its distribution and noting its great change- 
ableness and instability. 

The pain sense is probably the one most frequently reported. In 
fact, more or less pain is complained of in every case of true hysteria. 
To attempt to give a complete description of the pains of hysteria would 
be to write a volume upon every kind of pain known to the human 
mind. 

The pains of hysteria may be of every sort and of every degree of 
severity; they may be located in any or all parts of the body; and 
they may act exactly as any other sort of pain acts. Then how are we 
to determine the hysterical character of these pains ? Often we cannot. 
Less frequently we can do so only by their association with other symp- 
toms and conditions suggestive of hysteria, and still less frequently 
by certain peculiarities that in a few hysterics do characterize and dis- 
tinguish them from other forms of pain. 

In the head there is with the pain an occasional hyperesthesia. 
The patient dislikes combing of the hair. Often there is a distinct 
clavus or sharp circumscribed area of pain at the vertex, a |x>sition 
not commonly selected by headaches from other causes. Rarely thi- 
pain is dull and spreads over the whole cranium or is limited to one 
side. In such instances neurasthenia or migraine should be carefullv 



no 



THE NEURONIC DISEASES 



FIGURE 25. 




1 [ysterical anaesthesia. 



THE NEURONIC DISEASES IIT 

eliminated before a diagnosis of hysteria is made. With hysterical 
clavus, lasting several hours or days,- there is not unfrequently vertigo, 
nausea and vomiting. Remember that hysterical headache, whether it 
is vertical, occipital, temporal cr of the entire head, shows a tendency 
to be influenced by the mental condition of the patient. In this it differs 
from other forms of cephalalgia. 

Spinal pains are a part of the hysterical condition. I have not 
found them equally distributed along the entire spine so regularly as I 
have in neurasthenia. In hysteria they are more focal in character, a 
choice location seeming to be between the shoulder-blades. When 
tested by percussion or by the passing of a hot or cold sponge up and 
down the spine the patient winces or at least indicates suffering when 
certain spots are passed over. In this the trouble resembles the focal 
meningitis of the spine, from which it must be differentiated of course 
by other symptoms. 

Pains are frequently complained of in the region of the ovaries 
and mammary glands. In all cases of genuine hysteria these areas, the 
hysterogenic zones, are highly sensitive and may be painful upon pres- 
sure. I have seen hysterical men who suffered from sharp pain in the 
testicles, usually the left. Trunk pains, resembling intercostal neural- 
gia, gastralgia, cardialgia and even the cincture phenomenon of organic 
spinal disease, may be present. 

Pains are not frequently complained of in the extremities. Here 
the altered sensation more often assumes the character of numbness or 
"pins and needles." Once I saw in a young woman a painful toe that 
simulated gout. Under treatment it soon felt like a needle which the 
patient declared she had accidentally swallowed when an infant. Here, 
under suggestion, hyperalgesia was replaced by paresthesia. Cure 
followed further suggestion and the skiagraphic proof that there was 
no needle present. Mobius has described under the name akinesia 
algera a form of hysterical immobility caused by the pain produced in 
every form of movement, voluntary or forced. The pain is purely 
psychic in origin. It may involve every movement of the body and at 
times prove a most serious obstacle to treatment. 

Sensations of heat and cold, of formication, of alterations in size 
and strength, are much more common, in my experience, as hysterical 
symptoms in the extremities than are pains. This difference between 
the sensory phenomena of the trunk and the extremities is probably 
due to the psychic character of hysteria, the finer and more complicated 
physiology of the extremities having a more varied psychic representa- 
tion. The sensation of pain is more primitive and elemental than are 
the hallucinatory sensations like formication, worms, pins and needles. 

All of these sensory disturbances are of central or psychic origin. 
They may occasionally be awakened or localized by some form of 
peripheral irritation, but they are mental hallucinations. They arc the 
expression of the direct excitation of the pain-perceptive centers of the 
brain. 

Next to pains, so important are the paresthesias, hyperesthesias 
and anaesthesias in the symptomatology of hysteria that they must be 
considered a little more in detail. 



112 THE NEURONIC DISEASES 

Formication, the feeling of ants and worms crawling over the 
body, and numbness are probably the most frequent paresthesias. It is 
a question whether some of the strange delusions of the hysterical 
may not be due in part at least to internal as well as external forms 
of paresthesia. A patient who was a typical hysteric had the delusion 
that there was a fish in her head which swam about there and came 
forward to drink whenever she swallowed liquid. Hysterics not unfre- 
quently complain of toads in their stomach and of worms in their 
bowels, which delusions may well be due to visceral paresthesia. 

Perverted sensation is in the very nature of things psychic and is 
therefore almost pathognomonic of hysterical or Other forms of psycho- 
sis. It may be provoked by various peripheral stimuli, but the per- 
version can only be the result of central trouble. In this it differs from 
hyperesthesia and anesthesia which may depend upon peripheral 
nervous disturbance as well as central, and are not so necessarily indica- 
tive of a psychosis. 

Hyperesthesia and anesthesia, being merely degrees of sensory 
disturbance and not perversions, are not pathognomonic of a psychosis 
and therefore are less valuable as symptoms of pure hysteria. They 
may both be due to actual peripheral nerve disease and thereby be asso- 
ciated with probable hysteria. On the other hand, they may not repre- 
sent any actual organic disease at all, but may be entirely central in 
origin and therefore indicative of a pure psychosis. In the latter case 
their distribution, their favorite location, their variability and change- 
ability and their modification under the patient's ever-varying mental 
state indicate their purely hysterical origin. 

It is rare for hyperesthesia ever to be complete. It is more fre- 
quently seen in spots and circumscribed areas or in conjunction with 
certain viscera and deep structures like the muscles and fascia. The 
hyperesthesia frequently coincides with the hysterogenic zones, a fact 
which is made use of to initiate or check an attack of hysteria, by 
making pressure upon them. These hysterogenic zones on the anterior 
part of the body are the areas just under the mammary glands, just 
above the ovaries, along the sternum, at the outer end of the clavicle, 
at the lower, lateral edge of the thorax and at the vertex of the head. 
The spinous processes of the back are often hyperesthetic as well as the 
tip of the coccyx. The left side of the body being the sensitive side, 
hyperesthesia as well as anesthesia selects it most frequently when 
they are of psychical origin. 

The special senses also frequently submit to an hysterical ex- 
aggeration of their function. Flashes of light, flickerings and other 
visual phenomena are among the common signs of hysteria. An in- 
crease of the visual field (Freund) in all directions is much rarer than 
a diminution. The "tubular field of vision'' is a condition in which 
there is a constriction and the absolute area is the same, no matter at 
what distance it is measured. I have seen it once. Partial increase, 
however, with partial diminution and the increase of some of the 
color fields, which virtually amounts at times to crossing or reversal of 
the color fields, is a form of partial hyperesthesia that I have not tin- 



THE XETROXIC DISEASES 



113 



FIGURE 26. 




Hysterical anaesthesia. (After Thomsen.) 



114 l'BE NEURONIC DISEASES 

frequently seen. Double sight with one eye, not otherwise accounted 
for by optical conditions, is hysterical. 

Taste and smell and hearing may all be exaggerated. The hyper- 
sensitiveness of these nerves, however, is clearly psychic. The per- 
version of their function is probably more common in hysteria than 
is hyperesthesia. 

The ancesthesia of hysteria is clinically the most valuable of the 
sensory symptoms. It is the most frequent, is less intensely subjective 
than the others and can be examined with a higher degree of objec- 
tivity. Like the other sensory symptoms, it is purely psychic, as shown 
in its distribution and variability. As Bernheim well points out, all 
psychic anaesthesia, however, is not hysteria. Hemianaesthesia may be 
directly added to hemiplegia by pure psychic dynamism. It may occur 
from various causes in patients who are not the least hysterical. Hys- 
terical anaesthesia is observed in connection Avith all forms of sensation, 
special as well as general. 

The most common form of cutaneous anaesthesia is that which 
involves one entire half of the body, hemianaesthesia. Next in fre- 
quency is that which is limited to the conscious segments of the body, 
the hand, the forearm, the arm, the leg, the top of the head. This is 
the glove-type or drawers-leg type of anaesthesia. Its boundaries usu- 
ally correspond with the transverse folds and joints of the body or with 
the so-called transverse amputation lines. 

Both the hemianaesthesia and the glove-type reveal the psychic 
nature of hysteria, for they correspond to the mental conceptions of the 
parts of the body and not with the anatomical distribution of the sen- 
sory nerves. 

The least frequent of all the forms of anaesthesia is that in which 
the insensibility is scattered in patches or circumscribed areas about the 
body. And yet even this form is not in correspondence with the strict 
arrangement of the sensory nerves. It is bizarre and irregular. Its 
areas are located in and about the hysterogenic zones. It is deter- 
mined by such numerous local influences upon the patient's mind as 
pressure from the clothing, exposure, physiological function. Its bor- 
der lines are sharper than are the border lines of organic anaesthesia. 
This diffuse form of anaesthesia should be always most guardedly pro- 
nounced upon, for it is the type that is most liable to cause hysteria 
to be erroneously diagnosed for such organic troubles as multiple 
sclerosis, polyneuritis, etc. It may even occur with these diseases. 

This cutaneous anaesthesia is chiefly a pain anaesthesia, the tactile 
sense being normal or only slightly blunted. It closely resembles in this 
respect the dissociated sensory phenomena of syringomyelia. It is fre- 
quently tactile, however, and then the pain sense is alsc usually entirely 
absent. Occasionally the touch sense is merely blunted, hypccsthcsia. 
It is never merely delayed as in certain organic troubles. 

Loss of, or diminution of, the temperature sense, thermanaesthesia, 
may be observed. 

All these superficial forms of sensory disturbance are met with 
in the mucous membranes as well as in the skin. The mouth, the 
vagina, the rectum may all be involved. The superficial reflexes will 



HE NEURONIC DISEASES 



US 



FIGURE 27. 




Hystcric.il hemianaesthesia. (After Charcot.) 



n6 



THE NEURONIC DISEASES 



FIGURE 28. 




Hysterical anaesthesia. (After Charcot.) 



THE NEURONIC DISEASES 



117 



be correspondingly involved, though at times a reflex response may be 
obtained in spite of anaesthesia, if the test is made suddenly and when 
the patient is not expecting it. The deep sensations, as those of the 
viscera, the joints, the fascia, are also subject to anaesthesia. Hysterical 
astereognosis and loss of the sense of position may be present from 
implication of the muscular sense and other deep senses. 

The special senses undergo hyperesthesia and anaesthesia. Upon 
this many of the curious phenomena of hysteria depend. The visual 
disturbances are the most common and important among the special 
senses. Complete amaurosis is very rare and loss of central visual 

FIGURE 29. 




— : 1^- f - 

Hysterical contraction of the visual fields. Private case. Charts drawn by 
Nance. 



acuity almost never occurs. Usually there is a more or less concentric 
narrowing or contraction of the field of vision, which of course must: 
be determined by a perimetric examination. The perception of colors 
may be lost or diminished, or the limitations of the color fields may be 
reversed so that they will overlap. These phenomena are usually more 
marked on one side than on the other. When unilateral the eye affected 
is usually the one on the same side as the cutaneous anaesthesia, which 
is mostly the left. Whenever the order and extent of the fields for 
white and colors are reversed, the evidence is positive of the existence 
of hysteria. It cannot be simulated. It does not occur in any other 
ocular disorder. Ring scotomata are particularly suggestive of a 
psychoneurosis. That the loss of vision is mental and not organic is 
shown by the fact that, unlike organically blind people, these patients 
avoid obstacles placed in their way. It can also be proved to be mental 
by the use of the stere iscope, by prism- ingeniously arranged and by a 
box in which the lines of vision from the eyes are made to decussate by 
means of small mirrors. The preservation of the pupillary reflexes in- 
dicates its non-organic character, and even though the pupils are at" 



n8 



THE NEURONIC DISEASES 



fected, as they sometimes are by hysterical spasm, their appearance 
and mode of action is not at all in correspondence with an organic loss 
of the visual sense. All forms of anaesthesia may attack the retina, so 
that there may be hemianaesthesia or quadrant anaesthesia or focal and 
diffuse spots of anaesthesia. The same may be said of the achromatop- 
sia or dyschromatopsia that may exist. It is to be remembered that 
ocular hysteria is common in children and men. Organic disease of 
the eye may accompany the functional disturbance. 

The taste and hearing are sometimes lost on one or both sides. 
The alterations of taste explain the readiness with which these patients 
will resort to such filthy habits as swallowing urine and eating dirt. 
Moreover it accounts for their hallucinations and absurd declarations 
in regard to the articles of food that are given them to eat. Hysterically 

FIGURE 30. 

LEFT 





Ring scotoma in a hysteropic boy. (After Wood.) 

deaf patients do not as a rule incline their head in an effort to hear like 
those affected with organic deafness. Osseous conduction is usually 
absent. There is often cutaneous anaesthesia in and about the meatus 
of the deaf ear. 

When the olfactory sense is involved, the patients do not com- 
plain of disgusting odors and they may even reverse normal opinion 
and seem to enjoy that which nauseates the attendants. Hallucina- 
tions and illusions are common enough here. 

It is a curious fact that sometimes the patient himself is not 
aware of his various anaesthesias and only realizes them when they are 
demonstrated by the examining physician. Their instability, peculiar 
distribution, sudden transference and general bizarre character make 
them important, almost pathognomonic symptoms of hysteria. Janet 
thinks they are but the objective manifestations of the contraction of 
the field of consciousness. 

All forms of motor disturbance may be observed in hysteria. 
Spasms, both tonic and clonic, arc more frequent than are the con- 
tractures, pareses and paralyses. These disturbances are never as com- 



THE NEURONIC DISEASES IIQ 

plete as, nor do they simulate identically, the organic motor disturb- 
ances. Their psychic origin is noticeable in their peculiar functional 
character, their incompleteness, their localization and distribution, their 
duration and their instability and abrupt changeability. The absence 
of other distinguishing symptoms that accompany organic motor dis- 
turbances indicates the psychic or hysterical nature of these. For ex- 
ample, respiratory spasm of hysterical origin is not accompanied by the 
usual signs of the need of air ; hysterical paralyses do not exhibit the 
typical flaccidity or spasticity, the atrophy, the reflex and electrical 
changes which are associated with the organic paralyses. The motor 
disturbances of hysteria are due to an alteration in the patient's con- 
cepts of motion. Just as a hysteric really feels and sees and hears but 
does not know that she does, so she really can move her limbs but fails 
to do so because she does not know that she can. For this reason it 
has often been erroneously taught that aboulia, or paralysis of the will, 
was the underlying factor in hysteria. In the words of Paget the hys- 
teric says "I cannot" ; it looks as if she "will not" ; in reality, she cannot 
will. Such a view of hysteria is, however, not correct. There is plenty 
of volitional power, as is so often shown by the persistence and deter- 
mination with which the patient carries out her special plans and de- 
sires. The aboulia of hysteria is only an apparent loss of will power 
due to a perversion of the appropriate concept of motion. Suddenly 
restore this lost concept by suggestion, or mental shock, and the aboulia 
will vanish. 

Chief among the hysterical spasms, if indeed it is to be regarded as 
the result of a spasm and not a form of paresthesia, is the well-known 
globus hystericus. The patient complains of a lump in the throat, a 
ball which may or may not seem to have risen from the stomach and 
which feels as if it were held in the grip of the pharyngeal muscles. 
This sometimes produces great distress and together with spasm of the 
glottis may cause so severe a spell of choking as to call for the opera- 
tion of tracheotomy. The muscles of respiration are frequently in- 
volved. In fact the emotional and respiratory spasms are among the 
most common motor disturbances of hysteria. The crying and laugh- 
ing, often so meaningless, are of this nature, as likewise are the attacks 
of singultus (sometimes epidemic according to Oppenheim, Abelcs and 
others), eructation, of yawnings and of sneezing. Instead of tachypnoea 
there may be aphonia from implication of the vocal cords. Hysterical 
aphonia and aphasia are both common, especially the former. Cough 
(tussis hysterica), when present, is peculiar. It is dry, short and sharp 
like a dog's yelp and is absent during the night. Twitching of the eye- 
lids, blepharoclonus and blepharospasm, with photophobia and water- 
ing of the eyes may be present, but is more common in neurasthenia. 
a disease which often complicates hysteria. 

Any of the voluntary muscles of the body may be subject to hys- 
terical spasm. Twitching and convulsive movements, all forms of vio- 
lent motion, tonic as well as clonic, may attack the limbs and hurl them 
about or hold them in a rigid attitude. When the back muscles are in- 
volved there will be Opisthotonos or rhythmical arching 01 the body. 
All degrees of muscular spasm arc possible, and this, taken in con- 



120 



THE NEURONIC DISEASES 



junction with the fact that the movements are the same, only more 
vigorously performed, as normal voluntary movements, has formed 
the basis of an attempt to classify them. Even with the most violent 
spasms, consciousness is never entirely lost ; usually it is entirely 
present, though in the more severe cases it is clouded and disturbed 
with hallucinations. A curious hysterical phenomenon is the Saltatoric 
spasm, first described by Bamberger in 1859. It is rather more fre- 
quent in males than females. The symptom appears usually suddenly 
and consists of very rapid alternating contractions in the flexors and 
extensors of the legs, causing the patient to jump entirely off of the 
floor. It occurs only on attempts to stand and ceases when the patient 
sits or lies down. Scarcely ever does it attack the arms, and then only 
slightly. Hopping, jumping and running around, whenever he touches 

FIGURE 32. 




Major hysteria. (After Hamilton.) 



the floor, is the predicament of the patient. The spasm is clonic and 
involves ehiefly the calf muscles. Gowers, Kast and Eilenmeyer be- 
lieve it is a form of reflex. I am inclined to regard it as hysterical. 

A consideration of the various periods of a grand attack: of hys- 
teria, as outlined by Charcot, forms an interesting commentary upon 
the psychic nature of the disease and upon the manner of the, action 
of the mind. In the first stage, the consciousness being fully awake 
and realizing that something dreadful is impending, there are charac- 
teristic prodromes. There is irritability of temperament, fear, depres- 
sion of spirits, palpitation of the heart, restlessness, anxiety, aurse from 
the ovaries or stomach, paramnesia? of various sorts (tinnitus) eructa- 
tions, globus, visual mistiness and. partial clouding of the mental facul- 
ties. After this premonitory stage follows in a short time the second 
or epileptoid stage. The consciousness becomes still more obscure and 
perceiving, as it were, its gradual loss of inhibitory control over the 
lower or subconscious faculties, it becomes involved in a struggle in 
which it is more or less conquered. In almost every particular, except 
the suddenness of onset and the completeness of unconsciousness, this 
second stage of grand hysteria resembles an epileptic attack. It has 
been called hystero-epilepsy. It is pure hysteria and has nothing in 
common with epilepsy but the resemblance. The patient falls to the 



THE NEURONIC DISEASES 



121 



ground, the eves are closed, the head is rigidly drawn backward or to 
one side, the muscles of the jaw are clenched, the tongue is protruded 
and bitten, the face is red and then cyanotic, asphyxia seems imminent, 
arms and legs are strongly extended and adducted, the hands are 
tightly closed, the back is arched and the whole body is rigid and stiff. 
In a few minutes this rigidity passes off and a stage of clonic spasm 
follows. The face assumes horrible grimaces, the limbs and body un- 
dergo rapid alternations of rigidity and relaxation, the patient rolls 
from side to side or makes salaams or throws her legs into the air and 
does all kinds of absurd and purposeless things. She cries, screams, 
laughs, bellows, barks, scolds, yells and seems to be in a perfect de- 
lirium of mind and muscle. 

There is in all this a slight return of the mental faculties, but the 
consciousness is far from being awake, only realizing as it were its 

FIGURE 33- 




H vstero-epilepsy. Arc de Cercle. (After Richer.) 

powerlessness and want of control over the subconsciousness. It 
struggles to regain its normal ascendency, but failing to do so, the 
patient passes into the third stage in which the subconscious dominates 
and controls the physical movements, not in the delirious and spasmodic 
way of the unconscious epilptoid stage nor in the rational, purposive 
way of the fully awakened higher consciousness but in a hazy, semi- 
rational, dream-like manner that harmonizes perfectly in all probability 
with the ill-defined, ill-regulated, evanescent, incongruous multitude 
of hazy ideas floating en masse here and there through the patient's sub- 
consciousness. This is the period of the passionate (plastic) attitudes. 
The hallucinations of which the patient is the victim, may almost be 
positively suspected by the attitudes she assumes. Fear, auger, ecstasy, 
eroticism, meditation, religious emotion, jealousy, love, hate, are all 
marvelously depicted. The ecstatic and divine possessions of the 
mediaeval saints, nuns and monks, the enraptured attitudes often painted 
by the great artists in their pictures 'if the early fathers of the church. 
and all that class of tales, biographies, legends and art in which high 
and ecstatic emotionalism is represented, is now explained upon a 
hvsterical basis. 



122 THE NEURONIC DISEASES 

The hallucinations of the patient in this third stage of grand hys- 
teria may be modified by external stimulation through any one of the 
senses. She is in a sort of hypnotic state, much as a normal person is 
when half asleep. Inpouring impressions are received and acted upon 
as if they were original. 

Finally, as a last stage, there follows a quiet delirium as the pa- 
tient is emerging from her subconscious condition into one of full 
consciousness. In this terminal delirium certain animal hallucinations 
play the most important role. When the entire attack has passed off 
there may remain some disturbance of sensation, movement, etc., for a 
time. These attacks may last altogether from ten to thirty minutes. 
When they follow one another with great rapidity for several days, 
the condition is known as status hystericus. 

Comparatively few cases of grand hysteria, as described above, 
are seen in this country, or outside of France and the Latin countries. 

FIGURE 34. 




Hystero-epilepsy. (After Mills.) 

Here the attacks are more apt to be mild and the symptoms more or- 
ganic-like and localized. There may be slight premonitory feelings 
of depression and exaltation, irritability, restlessness and gastric sensa- 
tions, which, however, are hardly ever obtrusive enough to deserve 
the name of aurae as it is used in epilepsy. Then follows the emotional- 
ism shown by crying, laughing, screaming, attitudinizing. Pains and 
hyperesthesia are loudly complained of. Tremor and vibratory move- 
ments involve the whole or parts of the body. Even local paralysis and 
contractures may appear. 

All of these manifestations occur under complete consciousness, 
with more or less volitional preservation and with great changeability. 
A sudden change in the patient's mental state may cause them to change 
suddenly or disappear entirely and the attack be thus brought to an 
end. On account of this, willfulness and obstinacy seem to be at the 
bottom of the patient's doings, and the attendants becoming thereby" 
angry and impatient, she is created with some form of punishment. 
This is a serious error and shows that the attendants have no real con- 
ception of the nature of the disease. The harsh and painful methods so 
often adopted in the management of these cases produce their results 



THE NEURONIC DISEASES 



123 



not by reason of their punitive characteristics, but by reason of their 
influence upon the diseased mentality. 

The tremor of hysteria is peculiarly frequent and characteristic. 
It may involve the whole body or only the extremities. In the more 
common forms the oscillations (five to seven a second) are rapid, 
rhythmical and of large amplitude. The tremor may vary so as to 
simulate paralysis agitans, or it may assume the appearance of the 
jerking movements of multiple sclerosis, chorea or myoclonus. Hys- 
terical chorea is pure hysteria that is sometimes supposed to be chorea. 

Various forms of local paralysis or limited paresis are met with in 
hysteria. A close stud}' of the paralysis reveals its psychic origin, 
for it seems to be clearly due to a sort of aboulia, the loss of will power, 

FIGURE r?. 




Hystero epilepsy. (After Mills.) 



however, being itself due to the loss of mental conception of motion. 
It disappears under ether narcosis and electrical stimulation. It i> 
changeable and is never accompanied by atrophy or other trophic symp- 
toms. Instead of being a complete paralysis it is more often a kind of 
loss of energy. The grasp of the hand is feeble, but changes even while 
the attendant is holding the hand. The weakness is volitional in origin, 
as shown by the fact that automatic movements are often retained. 

All forms of organic paralysis, monoplegia, hemiplegia and para- 
plegia may be simulated in hysteria. The monoplegias are probably 
the most frequent, the hemiplegias the lea- .inic paralysis is best 

differentiated by exclusion, though as a rule there will be slight varia- 
tions in hysterical paralysis that upon very careful examination will 



I2 4 



THE NEURONIC DISEASES 



render its diagnosis usually easy. For example, hysterical hemiplegia 
scarcely ever includes the face and tongue, as organic hemiplegia usu- 
ally does ; and the contracture upon the hemiplegic side may be in the 
reverse direction from what it would be in organic disease. In the 
consideration of the various organic paralyses, further details in regard 
to their differentiation from the hysterical form will be mentioned. In 
all these paralytic conditions the knee-jerks are never lost; as a rule 
they are increased. 

Hysterical aphonia is a paralytic symptom so common as to de- 
serve special consideration. The voice being so closely involved in the 
mentalization of the patient, its loss is one of the most frequent forms 

FIGURE 36. 




Hystero-epilepsy. (After Mills.) 

of hysterical paralysis. The paralysis is usually sudden in onset, com- 
plete, and involves both vocal cords. It is volitional in origin, as shown 
by the fact that in singing, counting or in any other form of automatic 
vocalization, as well as in coughing and hawking, it is sometimes mo- 
mentarily restored. Usually the patient can only whisper. At other 
times the paralysis is not so complete, the voice being altered and 
rendered harsh and unnatural. In rare cases even the power of whis- 
pering is lost. This is known as hysterical dumbness or mutism. Un- 
like aphasics, a hysterical mute preserves more naturally her panto- 
mimic actions and cannot even articulate a single word. Close to 
hysterical mutism, either preceding or following it. is hysterical stutter- 
ing. Hysterical deafness has also been observed with the mutism. 

The ocular paralyses of hysteria are the subject of much dis- 
cussion. Ptosis, or pseudoptosis, due to a spasm ^i the orbicularis 
palpebrarum is not uncommon. Sometimes the eyelid is kept widely 
open by a spasm of tin levator palpebrae. The diagnosis of these con- 
ditions from organic paralysis is difficult, but powerful psychic sug- 
gestion, with the aid of electricity, will often diagnose correctly and 
cure the paralysis. The muscles of the eyeball are rarely paralyzed. 
( )ppenheim says they are generalh simulated by contracture of the 
antagonists, as, for example, spasm of the internal rectus, causing an 



THE NEURONIC DISEASES 



125 



appearance of paralysis of the externus. He further declares that in 
his experience a true hysterical paralysis of the Ocular muscles never 
occurs. It is admitted by others, however, that a myosis, paralysis of 
the muscles of accommodation, and pupillary rigidity may occur. 
Monocular diplopia or polyopia may result from closure of one eye. or 
defective accommodation. It may be associated with micropsia or 
macropsia. As in all hysterical paralyses, these of the eye are char- 
acterized by their lack of permanency, their alteration under psvchic 
influence and their association with other hysterical manifestations. 
Dysphagia, with or without disturbance of articulation, is an oc- 
casional symptom of hysteria. It is due to paralysis of the velum 



FIGURE 37 




Hysteric flexion contracture of 
one leg. (After Richer, taken from 
Tourette's work.) 

palati and deglutitorj muscles. It is generally complete and must 
therefore be most carefully distinguished from organic paralysis. 

Diaphragmatic paralysis is rare in hysteria, though it is often 
simulated by malingerers. Cases have been reported by Gilles de la 
Tourette, Petrazzini and others. It i< very alarming sometimes. Ac- 
cording to Wernicke, there is an insufficiency of the diaphragm, which 
is common in both hysteria and neurasthenia. In my opinion it belongs 
to the latter neurosis, which, as is well known, sometimes complicates 
hysteria. Paralysis of the bladder is very rare. The retention of the 
urine and the occasional dysuria are due to hysterical spasm of the 
sphincter vesicae. 

Disturbances of the Alimentary Canal. — Loss of appetite, anorexia 
hysterica, is sometimes a serious condition, for if not overcome after 
a time, it will lead to inanition and even death. It sometimes altera 
with excess of appetite or bulimia. Eructations of gas from tin- stom- 



126 THE NEURONIC DISEASES 

ach are not uncommon, especially in cases of hystero-neurasthenia. 
Vomiting is more frequently a purely hysterical manifestation than are 
the eructations. Mucus and saliva are expelled, usually with the food 
that has just been swallowed. In spite of this the appetite and general 
physique do not fail. Stercoraceous vomiting may occur and according 
to Fazio may be spasmodic or paralytic in origin, but is not due to sim- 
ple antiperistalsis. The vomiting may not be so purely a hysterical 
symptom in some cases as it is the result of the ingestion of nauseous 
substances, like urine, taken purposely to provoke sympathy. As a 
rule vomiting is not a particularly dangerous symptom in hysteria, 
whatever may be its origin. 

Both constipation and diarrhoea are observed in hysteria. The 
former is so common as to have been considered a predisposing cause, 
chiefly through autointoxication. A temporary diarrhoea, after some 
violent emotion, may occur in hysteria as well as in some normal states. 

Abdominal distension, known as meteorism and tympanites, with 
intestinal gurgling and borborygmus, occur in nervous people and may 
be very annoying in hysteria. The distension often subsides without 
the evacuation of the gas that caused it. 

Disturbances of the Circulatory and Vasomotor Systems. — In the 
paroxysm the pulse is apt to be accelerated. When there is syncope it 
is retarded. Cardiac palpitation is usually a mere subjective sensation 
and may be associated with difficulty of respiration. Under high emo- 
tion the palpitation may be real. The purse often remains normal. 
Spontaneous haemorrhages from various parts of the body of a hys- 
terical patient should be looked upon with suspicion. As a rule it is 
brought on by secret means to provoke attention. This is confirmed 
by the fact that such haemorrhages rarely occur from the internal organs 
which are beyond the reach of the patient's machinations. It is de- 
clared, however, upon good authority, that spontaneous bleeding from 
the forehead, breast, foot and other superficial parts of the body does 
occasionally occur. Metrorrhagia may be very profuse, but curiously 
the general health is but little affected. 

Much more common, reasonable and objectively demonstrable is 
the occasional local asphyxia sometimes associated with hysterical 
anaesthesia. Oppenheim once excised a piece of muscular tissue from 
a hysteric without any. bleeding. Vasomotor spasm is the explanation 
of this phenomenon. Pallor, flushing, cyanosis may all be observed, 
often in rapid alternation in the same patient. Souques has reported 
a case of hysterical Raynaud's syndrome, in which mere suggestion 
with a placebo caused the paroxysms of local asphyxia, which up to 
that time had averaged eight a day, to disappear entirely. Of course. 
in this hysterical type of Raynaud's disease, or syndrome, gangrene 
does not occur. (Edematous-like swellings, non-pitting, with decrease! 
local temperature, are sometimes seen. On account oi the (edema, 
pain on movement, etc., a hysterical joint may closely simulate joint- 
disease. The vasomotor disturbances may be responsible largely for 
the associated hyperidrosis, polyuria and even diabetes insipidus that 
occasionally take place. Hysterical skin affections are vasomotor in 
character. Gangrene has thus been seen to follow an urticaria, an cry- 



THE NEURONIC DISEASES I2J 

thema or more frequently pemphigoid blebs. Occasionally a gasteri- 
form eruption was the first symptom (Van Harlingen). 

The very nature of the disease, with its exalted emotions and 
imagination, would presuppose frequent disturbances in the sexual 
sphere. Doubtless this is the reason why the disease was so long re- 
garded as primarily due to sexual aberrations. The effect was mis- 
taken for the cause. Impotence and loss of sexual desire may be due 
to local anaesthesia. With a local hypersesthetic condition, or without, 
there may be abnormal desire amounting almost to nymphomania or 
satyriasis. Perversions and semi-hypnotic delusions in this sphere are 
not only possible, but are so common that no physician who regards 
his own comfort and reputation would think of examining a hysteric 
without the presence of a third party. 

Hysterical fever has been reported. As a rule it is the product 
of some form of deception. If it does occur it must be exceedingly 
rare. Hysterical attacks as a rule do not occur during the rise of the 
temperature. If changes in the pulse, respiration and renal secretion 
accompany the elevation of temperature, there is probably some obscure 
inflammatory -condition present. However, pure hysterical tempera- 
tures of 108 and 113 degrees F. have been recorded. A large question 
mark is to be put after the statement that Teale once found the tem- 
perature in a hysterical patient 122 degrees F. They are said to be 
characterized by large daily curves, to be but little influenced by the 
usual antipyretics, and to vary considerably when taken in different 
parts of the body. 

Pathology and Pathogenesis. — Much confusion surrounds the 
pathology and pathogenesis of hysteria. This is not because we have 
not complete data upon the disease, but because there is so much differ- 
ence of opinion as to the nature of psychic processes, both normal and 
abnormal. It is practically universally admitted nowadays that hysteria 
is a psychic manifestation with secondary neuro-muscular phenomena. 
It is primarily and essentially a psychosis. This psychosis is dependent 
of course upon the nature and course of the patient's individual ex- 
periences as brought to her through and by way of her five senses. 
Hence the role played by these senses in the causation of the disease 
and the long list of physical etiological factors that have hitherto been 
assigned at various times as the cause of hysteria. Up to the present 
time the pathology of hysteria has been made to include almost every 
possible alteration in about every possible organ and tissue of the body. 
One thing is certain, namely, that there are no constant pathological 
findings of any sort, and in all of the cases there are no changes in the 
central nervous system upon which a pathology can be erected. 

For this reason some deny that hysteria should be considered as 
a disease at all, looking upon it as a mere mental and nervous disturb- 
ance caused by the changes and diseases in any or all of the tissues of 
the body. 

On the other hand, some authorities regard it as the result of some 
hypothetical changes in the molecular substance of the nejve cells, 
causing them to manifest an abnormal functional activity, which clas 
fies hysteria as a dynamic disease without discoverable lesions. 



128 THE NEURONIC DISEASES 

In both of these explanations it will be noted that a physical basis, 
a pathology in the general sense of the word, is assumed for the dis- 
ease. It is a strange fact that the great variability, instability and sud- 
den changeability of the clinical manifestations of hysteria have not 
long since led the authorities to relinquish the idea of a physical basis 
for these changes. So materialistic is the average trend of thought 
that men find it hard to conceive of a disturbance of mentality without 
an underlying change of physical structure. This is scarcely to be won- 
dered at, for logically it would seem to be a necessity that every change 
of action presupposes a change of some sort in the acting substance. 
And yet there are ways by which activities may be changed and the 
underlying substance remain both physically and functionally undis- 
turbed. This is true not only in certain abnormal states, but is open 
to daily observation in perfectly normal states. Mental activities are 
complex in character and depend upon the play of their elementary 
constituents upon one another. These constituents may be acting in- 
dividually in the way that they should in all their normal perfection, but 
by means of an exaltation of some and a diminution of others or even 
by a simple rearrangement among them, the resulting complex and 
final activity may be very different from what was expected, or be sud- 
denly changed from what was at that moment in performance. 

A rough illustration may make this clearer. Suppose in a great 
railroad office all the employes are doing their usual duties in their 
usual way ; the great complex system will move in the usual way. The 
elements of the system, the individuals, will be working normally, and 
so the sum total of activities, the working of the entire railroad from 
end to end, will be normal. Suppose, however, some unusual factor is 
introduced among the activities of the individual employes ; suppose 
the president of the company or the manager, with all his authority 
to command, should give to one of these individual employes an erratic 
order to pass on over the system. The employe takes the order and 
does with it in his usual way what his chief told him to do; so does 
the next employe and the next; until finally the whole system is sud- 
denly disturbed in its usual routine of activity. The individuals, even 
the chief, were normal in structure, were well within the limits of their 
functional activity, and yet by an unusual play of these activities as 
individuals upon one another, there has resulted a most unusual work- 
ing of the entire complex activity of the whole system. 

Hysteria is a psychosis primarily and essentially. It involves in 
its last analysis a disturbance of the mental faculties — namely, the 
memory, the imagination, the will and the intellect. These so-called 
faculties, as well shown by that great teacher of modern physiological 
psychology, Wilhelm Wundt, are not actual entities or things with a 
physical habitat in the brain or elsewhere. They represent merely 
processes or forms of activity. They are merely convenient names 
for particular kinds of complex and compound movements. Accord- 
ing to Wundt, sensations and feelings are the primary and only ele- 
ments of all psychic manifestation. These sensations and feelings are 
dependent, of course, upon the physical changes in the nerve cells and 
fibres. These sensory and aesthetic phenomena combine or separate 



THE NEURONIC DISEASES I2Q 

among themselves in such a way as to produce that complex activity 
which we denominate the mind. The feelings, by becoming stronger, 
develop into emotions ; emotions overflow into muscular action if they 
are strong enough, and we call the process volition. Percepts are 
awakened by sensory stimulation and being brought into juxtaposition 
•or combined with other percepts form concepts. The comparing and 
contrasting of concepts is the process that underlies imagination, un- 
derstanding and judgment. 

Thus the whole mind is formed by the interplay of certain ele- 
mentary processes based upon sensation and feeling. These sensations 
and feelings may, of course, be disturbed by physical lesions in or 
about the nerve elements and the processes which underlie psychic 
action will be disturbed. 

This is the explanation of the way in which physical causes often 
give rise to hysteria, as well as to many other forms of mental trouble, 
such as polyneuritic psychosis, the psychoses of the infectious diseases, 
etc. But it is evident from Wundt's point of view or from the stand- 
point of modern voluntaristic psychology, that the mental faculties, 
so-called, may be disturbed by a disturbance in the mere interplay of 
the elementary, constituent processes that make up these faculties. 
These elementary constituents may not necessarily be abnormal indi- 
vidually, but if some of them be thrown into a state of unusual activity, 
the routine balance between them ail is so far disturbed as to cause a 
marked disturbance in the sum total of all their activities — namely, the 
mind. This explanation makes of hysteria a psychic disturbance de- 
pendent upon either physical or functional causes. The physical causes 
may lie in disease of the ultimate nerve elements, thus changing the 
elementary sensations and feelings that form the ultimate substrata of 
mind. ( )n the other hand, the functional causes may reside in an 
unwonted disturbance in the usual interplay of what may be quite 
normal sensations and feelings. 

Among the physical causes there may be found all sorts of lesions 
giving rise to hysteria. For this reason physical diseases of all kinds 
may provoke among those neurotically unstable an outbreak of hysteria. 
On the other hand, fright, sorrow, excess of joy, mental strain, may 
develop into hysteria in those neurotically unstable, not because these 
mental states are abnormal, but because they are so unusual as to dis- 
turb or at least represent a disturbance in the usual form of mentaliza- 
tion. No explanation of hysteria, in which disease there is admittedly 
no pathological findings, so harmonizes all the clinical phenomena and 
shows the half-truth contained in most of the explanations hitherto 
offered, for example, the old view that it was due to a paralysis of 
the will is true in part only. In some cases aboulia is present because 
the psychic process which we call the will and which is a product of 
the emotions, which emotions in turn are dependent upon the elemental 
feelings, is disturbed by the disturbance in these underlying proces 
Certain feelings are too weak or too strong; the corresponding emo- 
tions have caused the rise ( >f weak or altered motives; the resultant 
motor activity fails entirel) or is entirely perverted, [anet speaks of 
a "contracted consciousness" underlying hysteria. In some cases this 



I30 THE NEURONIC DISEASES 

may be ttue, just as the volition process may be rendered paretic. 
Others have thought that hysteria was due to an excess of mental 
inhibition. It is, in some cases. Still ethers find that emotionalism and 
an excess of imagination enter most largely into its pathogenesis. In 
some cases they undoubtedly do. And finally, not a few believe that it 
is merely the result of a vicious education and discipline in a neu- 
ropathic and unstable individual. In a large percentage of cases this 
also is most emphatically true. 

In all of these views, however, it will be remarked that the trouble 
is primarily a pure psychosis. The explanation which we have given, 
based- upon a rational and physiological explanation of mind, affords 
the best generalization for the harmonizing and clarifying of all these 
apparently diverse but really disjointed parts of one and the same 
view. 

Diagnosis. — In an ordinary, uncomplicated case, hysteria is not 
difficult to detect. The large majority of the cases, however, are not of 
the ordinary type or uncomplicated ; hence the diagnosis of hysteria 
is nearly always a matter demanding caution, thoroughness and experi- 
ence. It should always be diagnosed by the exclusion of all other pos- 
sible functional and organic diseases ; and in arriving at the diagnosis 
the psychic origin of hysteria should never be lost sight of. Even 
though the most careful and experienced physicians may be at times 
entirely at sea, the remembrance of the two facts just stated will go 
a long way toward making a diagnosis accurate. 

The mental origin of the motor, sensory and other symptoms of 
hysteria can nearly always be determined by the character and loca- 
tion of these symptoms and their alteration when the patient's attention 
is distracted, or his mind is put out of action, as it were, by chloroform 
or ether narcosis or hypnotism. An experienced examiner sometimes 
learns to detect hysteria almost intuitively, and this is not altogether 
surprising. Psychic manifestations of all sorts, or rather symptoms 
of all sorts that owe their origin to the mind of the patient, when 
collected and presented en masse, present a more or less characteristic 
picture differing from a collection of symptoms that owe their origin to 
simple organic changes in the nervous structures. The voluntaristic 
explanation of mind — namely, that it is merely a term to cover certain 
interdependent and interrelated processes among the elementary sensa- 
tions and feelings — accounts for the variability, distribution, change- 
ability and other peculiar characteristics of the symptom-complex of 
this psychic disease, hysteria, and emphasizes, on the other hand, the 
fixity, the anatomical distribution and the greater permanency and 
continuity of the symptoms of the organic diseases with which it is 
liable to be confounded. 

The psychic nature of hysteria makes plain why it is so often 
associated with organic diseases. For its activity, mind is dependent 
upon the activity of its primary elements, the sensations and feelings^ 
and these in turn are dependent upon the action of the histological 
nerve and other tissues of the body. Given an organic disease or dis- 
turbance of any kind anywhere in the body, and it is only a question of 
temperament, time and severity of this disease before a psychic dis- 



THE NEURONIC DISEASES IJI 

turbance will be provoked that may eventuate in a more or less severe 
attack of hysteria. One must not get the idea from this that hysteria 
is only a mental disturbance symptomatic of some organic disease, 
for such a notion would only represent a half truth. The mind is the 
result of two sets of underlying factors. On the one hand it is de- 
pendent upon nerve integrity and their normal sensations and feelings ; 
but on the other hand it is a process, a mere form of activity, dependent 
upon the normal interplay of the elementary processes of sensation and 
feeling. Hence, not all cases of hysteria are the product of gross 
organic diseases or are even associated with them. The association of 
the two diseases may obtain even without any relationship other than 
the mere association. All these facts must be taken well into account 
when differentiating hysteria from organic diseases and emphasize the 
importance of diagnosing the hysteria by the exclusion of every other 
possible disease. It is safer to overlook a hysteria than it is to pass 
organic symptoms as being hysterical. The condition of certain organs 
that are entirely beyond the control of the mind, as, for instance, the 
pupils, the heart and respiration, etc., may all be invoked to exclude 
hysteria. 

Probably the disease that is most frequently mistaken for hysteria 
is multiple sclerosis. Indeed, Westphal described a general neurosis, 
classified by Charcot and his school as a form of true hysteria, which 
could not be distinguished from multiple sclerosis either in its course or 
its symptoms, and which he called pseudo-sclerosis. True multiple 
sclerosis, however, may be distinguished from either hysteria or West- 
phal's pseudo-sclerosis by the presence of nystagmus, the condition of 
the optic nerve, the voluntary intentional tremor and the absence of 
psychic influences. The scanning speech of multiple sclerosis is more 
uniform and consistent than is the irregular speech sometimes observed 
in hysteria. In the latter disease some words are scanned and others 
are merely jerked out irregularly, quickly or slowly. The paraplegia 
of multiple sclerosis usually reveals a suggestion of spasticity, and 
clonus when present is absolutely involuntary, regular and intense. 
Remember, however, that hysteria and multiple sclerosis are often 
associated, and one must be careful to determine the symptoms that 
belong to either of the respective diseases. 

In brain tumor and cerebral syphilis there are symptoms that 
hysteria at times closely simulates. Moreover, both conditions may 
develop or at least be associated with hysterical phenomena. An error 
in diagnosis is therefore not uncommon. When there are the usual 
ophthalmoscopic signs of tumor or syphilis present, there can be no 
possibility of mistake. The headache of the organic troubles is differ- 
ent from that of hysteria in being more continuous, less sharp, more 
definitely localized and more prominent in the early hours of the morn- 
ing. With the cephalalgia of the organic diseases the mind is heavy, 
dull and apathetic, the countenance is expressionless and the pulse is 
retarded. There may be vomiting, Usually the other symptoms of 
hysteria are sufficiently pronounced to render a differential diagn 
clear. 

Hysterical paraplegia may be mistaken for the paraplegia of 



132 THE NEURONIC DISEASES 

myelitis. In the latter disease, however, the character and distribution 
of the sensory disturbance, as well as the bladder and rectal troubles, 
are sufficient to differentiate the two diseases. In myelitis the absence 
of all psychosis and the non-implication of the special senses are to be 
carefully noted. In the same way vertebral caries may be distinguished 
from hysteria, the sensitiveness of the former disease being more cir- 
cumscribed and less like a cutaneous hyperesthesia. 

Hysterical joints are often mistaken for arthritic disease. A 
careful examination of the joint for organic disease and of the patient 
for other hysterical stigmata will make the distinction clear. 

Hysterical pains ought not as a rule to be hard to differentiate 
from neuralgic pains or pains due to organic disease. One has but to 
remember that hysterical pain is a psychic phenomenon and therefore 
has no definite, fixed, anatomical location as have the pains of organic 
disease. On the other hand, the latter pains are not so susceptible to 
suggestion and diversion of the attention as are the psychic pains of 
hysteria. The other symptoms, both of hysteria and organic disease, 
are usually sufficiently in evidence to give very material assistance in 
the diagnosis. The pains of angina pectoris, cephalalgia, etc., may thus 
give rise to some confusion, but a careful application of the above 
principles in making the differential diagnosis will render the latter 
less difficult. 

The same may be said of the differential diagnosis between hys- 
terical and other forms of spasm, such as chorea, tetany, hystero- 
epilepsy, etc. The psychic complexion of the hysterical spasm is want- 
ing in the muscular phenomena of these diseases. 

Hysterical chorea, so-called, is a rhythmical movement, slower and 
more regular and not so incoordinated as are the jerkings of true 
chorea. Chorea magna, as I have explained elsewhere, is nothing but 
hysteria. 

Likewise, hystero-epilepsy is merely a severe form of hysteria in 
which the state of consciousness and convulsions resembles somewhat 
that of epilepsy. As there is no connection between hysteria and 
epilepsy but this superficial resemblance in a few cases, it would be 
well to drop entirely the use of the term hystero-epilepsy. It is as 
misleading and unwarranted as the term typho-malaria. 

Hysterical patients often become neurasthenic and vice versa, 
f >ccasionallv both troubles coexist in the same individual without any 
other connection. They both have their distinctive signs, which should 
always be carefully separated, as I have pointed out under the head of 
neurasthenia. 

Hysterical vomiting has not infrequently given rise to the errone- 
ous diagnosis of gastric ulcer, peritonitis, perforation and appendicitis. 
As a rule hysterical vomiting takes place so soon after the swallowing 
of food that the latter comes up quite unchanged. The absence of 
characteristic pains, elevated temperature, local tenderness and the 
general history and psychic nature of the trouble, will help to deter- 
mine easily the hysterical origin of the vomiting. 

Oppenheim points out that there are persons with a congenital 
(perhaps due to a developmental inhibition) or early developed weak- 



THE NEURONIC DISEASES 1 33 

ness in some particular part of the central nervous system, say the 
cerebellum, the medulla or particular cortical centers. Later in life 
these fail to functionate normally and disorders arise that are not 
strictly organic nor yet are purely hysterical. They may cause con- 
fusion in diagnosis, however, and should be guarded against. 

It is undoubtedly true that there is a strong inclination in hys- 
terical patients to practice deception. The exaggeration of the egotism 
with its necessary tendency to selfishness, the diminution in the inhibi- 
tory influence of the intellect and higher faculties and the consequent 
overactivity of the emotions, imagination and more elementary facul- 
ties, lead to the adoption of means and measures to accomplish ends 
that are not on a very high plane of justice and morality. A moment's 
consideration will convince one, however, that such deceptions are not 
criminal, as they would be if resorted to by a normal or non-hysterical 
person. Psychically the hysteric individual is a child ; mentally she has 
fallen back to an almost ape-like condition. To punish her in a vin- 
dictive spirit is both cruel and unjust ; to administer corporal pain 
with the hope of reforming her is useless and unscientific. Her mind 
is at fault. It is diseased. It works differently from the normal mind. 
It is under the control and influence of abnormal, strange and bizarre 
percepts and concepts. On account of this it may be acting most 
logically though the outward manifestations appear so extraordinary 
and provoking. The partial consciousness, the emotionalism, the 
screaming, the dramatic attitudes, the pugnacity may all be due to 
hallucinations and illusions of a frightful character, or to unusually 
active memory and imagination processes rather than to any nerve 
influences. The deceptions of true hysteria may be identical with the 
deceptions of malingerers. The difference between the two, however, 
lies in the underlying motive, and the cause and origin of that motive. 
In both it is a strong desire for some form of self-gratification. In the 
hysteric, however, it is usually a desire to gratify the mere personal 
ego, the love of self, sympathy, praise or some other form of spiritual 
self-aggrandizement. In the malingerer it is a desire for the acquisi- 
tion of some physical enjoyment, money, physical comfort, presents, 
etc. In this sense "hysterics" due to mere bad discipline, is a sort of 
mild form of malingering and being not the same as true hysteria 
may, unlike the latter, be treated at times advantageously by severe 
punitive measures. 

True malingering may be distinguished from true hysteria 1>\ 
various symptoms and measures, one of the best of which is chloroform 
or ether narcosis. Spasms of hysterical origin disappear and the 
sensory reflexes undergo change as the narcosis deepens. The paraly- 
sis may be tested by electricity, rlysteria being a psychosis, its mani- 
festations are so largely subjective in character that the examiner has 
but few objective signs by which to determine whether the patient is 
feigning or not. Nevertheless, it takes an exceptionally shrewd in- 
dividual to imitate all of the symptoms of hysteria or even a part of 
them, and to portray them with all their variability, changeableness, 
peculiar distribution so that they will continuously and constantly depict 
the picture of true hysteria. It is much easier to simulate organic 



134 THE NEURONIC DISEASES 

disease than it is hysteria ; so that if the simulator of hysteria be closely 
watched he will portray some of his symptoms, such as the paralysis, 
contracture, etc., in a way that will resemble organic disease rather 
than hysteria. The moment he does that his game is lost, for the 
symptoms which simulate organic disease, as, for instance, fixity of 
the paralysis, anatomical distribution of the anaesthesia, the vomiting, 
etc., do not fit in well with the other symptoms that he is feigning, and 
therefore it is evident that he is afflicted with no disease, either organic 
or functional. As I have before intimated, hysteria is always diagnosed 
best by the exclusion of all other possible diseases, because it is possi- 
ble for it to imitate all other diseases so closely ; and by a careful 
study of its general complexus rather than of its individual symptoms 
alone, because it is a disease of the personality, a psychosis, and not 
a disease of special anatomical structures. 

Prognosis. — The prognosis of hysteria in regard to life is good. 
In regard to recovery it is favorable for the attack, unfavorable for 
the general constitutional trouble. Hysterical conditions secondary 
to organic disease depend upon the removal of these organic lesions. 
The patient's congenital, physical and mental constitution, her age, 
her environment, all must be taken into account in determining the 
possibility of recovery. Medicine cannot hope to alter natural traits 
and inherited defects. It can do much, however, to mitigate their 
effects. Exciting causes it can often remove and consequent bad 
habits it can change. While a physician may offer a generally favorable 
prognosis in regard to particular factors of hysteria, as, for instance, 
the recovery from a sudden acute outbreak, he should frankly admit 
the probability of relapses and he must be very guarded in holding out 
hope of a complete and permanent disappearance of the disease. In a 
small number of cases, complete and permanent cure has been ob- 
tained. 

Treatment. — In the treatment of hysteria the guiding thought 
should always be its psychic nature. It is primarily a disease of the 
mind; in a large number of cases it is the result of a vicious habit of 
mentalization. This must be modified in some way before any real 
benefit from treatment can be hoped for. All forms of mental disci- 
pline are, of course, most effective in the impressionable period of 
childhood and their most brilliant results are secured in hysteria when 
adopted as prophylactic measures. Nevertheless, mental discipline and 
psychic treatment are imperatively called for by an hysteric at all 
times, whether young or old, whether during the convulsive attacks or 
during the intervals between them. In other words, first, last and all 
the time the sheet anchor in the management of hysteria is the psychic 
treatment. 

Typical hysteria occurs at all ages and in general exhibits itself in 
the same way in children as it does in adults. The treatment of the 
hysteria of childhood differs in no special respect from the treatment 
of hysteria in the adult. 

The hysteria of the adult is, as a rule, the expression of a peculiar 
form of constitution, and usually is preceded by certain premonitory 
indications in childhood that should put the physician on his guard and 



THE NEURONIC DISEASES 1 35 

urge him to give some advice to the parents as to the education and 
training of the child. Of course, the science of medicine cannot change 
the peculiar, inherited temperament which forms the background for 
the later hysterical outbreaks, but it its teachings are listened to and 
followed it can do wonders in forestalling these outbreaks and in 
keeping latent the ever-threatening tendency towards them. The whole 
field of child training, including a knowledge of psychology and mental 
development, of pedagogy and educational discipline, and of the 
psychological law T s of growth and evolution, is an exceedingly broad 
one. Either because parents, and alas, too often the family physician, 
are unwilling or unable to prepare themselves for so extensive a sphere 
of thought and activity, they fail to manage hysteria either from the 
prophylactic or the therapeutic standpoint. Unfortunately, much of 
the advice given under the head of the treatment of hysteria in text- 
books of even very recent issue is erroneous, because of the erroneous 
conception of the true nature of hysterical physical phenomena and the 
peculiar aberration those phenomena undergo in hysteria. Without 
occupying too much space here, let one illustration suffice. Nearly all 
the text-books suggest that hysteria, whether in the child or in the 
adult, is largely an aboulia and that therefore the patient's will should 
be strengthened in every possible way. As a matter of fact, the voli- 
tion of the patient is not paralyzed so much as it is perverted. Hys- 
terical patients only too often show a most vigorous will-power in the 
line of their perverted motives. Even when they are paralyzed or in 
a cataleptoid state, the will is not so much in abeyance as that it is 
working, perchance, too vigorously, in a direction entirely different 
from the ordinary channels. An overwrought imagination with 
reminiscences of intense fear, or of religious ecstasy or of sexual exalta- 
tion, may so absorb the patient's inner consciousness that the ordinary 
channels of mental activity are quite neglected and the patient is there- 
fore the apparent victim of such outward negative manifestations as 
anaesthesia, paralysis, etc. In the light of modern physiological psychol- 
ogy, so ably taught by Wundt, in which all mental phenomena are but 
composite psychical experiences resulting from the interplay and inter- 
connection of the two elementary processes, sensation and feeling, hys- 
teria like all other forms of psychosis, is the expression of an unusual, 
and so far unnatural, balance and harmony between these elementary 
processes. Its cure is the restoration and preservation of this balance, 
the establishment of the normal, or what is universally accepted as the 
normal, interplay of the primary processes or occurrences that go to 
make up the so-called memory, will, imagination and intellect, by the 
regulation and discipline of the physical elements, sensation and feel- 
ing. This conception of the nature of hysteria on the basis of modern 
physiological psychology, while it does not lessen the magnitude of the 
task involved in its prevention and treatment, gives to the task a more 
hopeful and rational ground whereon to work, than any explanation 
hitherto afforded. 

To ward off hysteria in one who has been born of neurotic parents, 
who shows in herself early in life a congenital neuropathic tempera- 
ment, or who has begun to reveal hysterical manifestations as the re- 



I36 THE NEURONIC DISEASES 

suit of a too close association with a hysterical mother or of a too 
close confinement to a predisposing environment, the indications are 
clear and involve the making of all such changes in the child's life as 
will change her psychic elements of sensation and feeling. Removal 
from home, the avoidance of too much sympathy, the regulation of 
studies and reading, the adoption of system in all life's activities, and, 
in fact, the employment of all measures, persuasive, punitive, educa- 
tional, social, disciplinary and of every other kind that will tend toward 
a regular, even, systematic, well-balanced mental and physical existence, 
in which no set of sensations, no set of feelings, no special faculty or 
organ of the mind or body is exercised at the expense of or more than 
any other. As most of these children, for example, are of the so-called 
artistic temperament with its preponderance of the imaginative and 
emotional faculties, they should be given games, studies and a general 
regimen that involve little or no exercise of imagination and feeling, 
but rather the intellect and reasoning faculty. The exercise of the 
imagination and emotions should not be prohibited entirely, as is too 
often done, for that merely reverses the unbalanced state of mental 
activity ; but they should be kept in partial abeyance by the giving of 
more work to the other faculties. 

Passing on to the consideration of the treatment of hysteria in 
the adult, the subject may be looked at from various standpoints. In 
the first place, the same sort of prophylactic treatment and discipline 
for the suppression of the disease is as applicable as it is in the child : 
its results, however, will not prove so happy because the adult cannot 
be controlled as a child can, and too often will not submit to proper 
self-discipline, and because in the adult the hysterical habit has usually 
become fixed more and more firmly m the course of the preceding years. 
Nevertheless, given a willing patient, prophylactic discipline along the 
lines suggested for neurotic children will do a very great deal in pre- 
venting the hysterical outbursts or in mitigating their severity when 
they have once broken forth. A volume might be written almost upon 
the details of such prophylactic treatment, for it would involve the 
consideration of all kinds of cultured and uncultured individuals and 
all forms of mental and physical activity known to the human race. 
The whole matter may be axiomatically slated in the one sentence, 
restore as far as possible the balance in the mental, moral and physical 
activities of the individual patient to whom the advice is being given. 

Physical diseases with which hysteria is so often associated must, 
of course, be removed. Ill health must be corrected with tonics, exer- 
cise, massage, baths, electricity, proper diet, sleep, etc. The mind must 
be appropriately ministered to as well as the body. All of which can 
be only suggested here on account of the vastness of the subject. 

In the second place, the treatment of the hysterical outbreaks. 
the paralytic and convulsive periods and their special symptoms, needs 
some consideration. The means at our disposal for combating this 
manifestation of hysteria are psychic, mechanical, medicinal. 1 am so 
convinced that hysteria is entirely a psychosis that I believe what 
benefit we obtain from such measures as are involved in all the 
hydropathic, climatologic, medico-mechanical and electric procedures 



THE NEURONIC DISEASES 137 

that have been recommended and are legitimately employed, is due to 
the effect upon the patient's mind. Of course, I do not mean by this 
that remedies applied to organic troubles with which the hysteria may 
be associated do not help to remove the psychosis, but they do it indi- 
rectly by removing the Organic disease which may be aggravating the 
hysteria. In a word, if a case is one of pure hysteria, free from all 
forms of organic trouble, the remedial measures that so often seem to 
banish the hysterical symptoms do so by directly influencing the pa- 
tient's mind. I take it that the entire treatment of pure hysteria is 
in its last analysis psychotherapy, whatever the means employed to 
influence the patient's mind. 

Even in an hysterical attack, therefore, the first thing to do is to 
win the patient's mind so far as possible. To do this the physician 
must first of all impress his personality, his mastery over the patient and 
the situation and his ability to handle the case, not only on the patient, 
but upon all those in her presence. He may have to be harsh or gentle, 
commanding or persuasive, indifferent or sympathetic ; each case will 
require its own method and the physician himself must alone decide 
what course of action to take. The patient's confidence must be ob- 
tained and after that there must be no temporizing with her. Ofttimes 
this can only be accomplished when the patient is away from her home 
and among strange surroundings. The hospital is the only place and 
the Weir-Mitchell method of seclusion, with a daily systematic pro- 
gram, modified, of course, for each individual case, is often the only 
means of obtaining the desired influence over the patient. The physi- 
cian must frequently impress the patient with not only his mastery, 
but also with the superiority of his mind and mental attainments. 
He dare not be boastful, but he must command the patient's respect, 
admiration and even awe. To do this he must often be a highly cul- 
tured man, for these patients are themselves frequently highly cul- 
tured. If the physician's mental endowments are such as to cause an 
accomplished hysteric to hold small respect for him, it is obvious that 
he will have but little of her confidence and so much the less mental 
control over her. It is well, therefore, to be able to meet the various 
tastes and mental endowments of these patients by a broad knowledge 
of science, literature and art. Moreover, out of such a broad knowl- 
edge, suggestions can judiciously be made in regard to the patient's 
reading, studies and artistic occupations. I make it a rule to include 
in the written program for the use of the nurse, the books to be read. 
the amusements to be indulged in, the general lines of conversation to 
be prohibited, and deem them quite as important as the directions which 
I give in regard to the medicines, food, baths, electricity, etc. 

Psychotherapy involves the question of the employment of hypno- 
tism and suggestion. What has just been said about the relationship 
of the physician to his patient is of the nature largely of suggestion. 
As to the use of artificial hypnosis there is some question. Hypii 
itself is a hysterical condition, and the substitution of one hysterical 
state for another may be inadvisable. Hence, hypnotism had better 
never be resorted to except as a final incisure after all other means 
have been tried and have failed. And yet it must be frankly admitted 



I38 THE NEURONIC DISEASES 

that for the removal of paralyses, anaesthesias and contractures, it is 
not only to be recommended but sometimes proves highly efficacious. 
One must be careful always to make appropriate post-hypnotic sug- 
gestions, so that the patient does not come out of her sleep in a worse 
hysterical state, with other and more serious stigmata, than those with 
which she entered it. 

I believe it makes very little difference in the treatment of hysteria 
as to the character, mode of application or time of employment of such 
excellent measures as baths, massage, electricity and gymnastics. The 
essential point is to insist upon their being taken with regularity and sys- 
tem, and not to allow the patient's mere whims and changeableness to in- 
fluence the use of them. To overcome her egotism and self-regard, to 
strengthen her higher mental inhibition, and to direct her thoughts into 
channels that lead away from herself and her own elementary sensa- 
tions and feelings, it is wholesome to render the taking of the baths, 
massage and electricity somewhat of a slight task, possibly unenjoyable 
but absolutely necessary. In this way cold baths, electric shocks, tire- 
some exercises, apart from their tonic and stimulating effect upon the 
physiological processes of the body, accomplish their happy effects 
when adopted as a part of the treatment of hysteria. 

In regard to the use of medicines in hysteria, it may be generally 
stated that they are of little avail. Hysteria is a psychosis which re- 
veals itself most prominently at times through the nervous apparatus ; 
hence it is sometimes called a psychoneurosis. This neurosis is seen 
in such symptoms as the muscular spasms, vasomotor disturbances, con- 
tractures and such automatic acts as laughing, crying, etc. To reach 
such conditions the antispasmodics are sometimes useful. Valerian and 
zinc are the best in the list. Asafoetida, the bromides, quinine, sumbul, 
methylene blue, may all be tried, but without psychotherapy will usu- 
ally be found wanting. Narcotics, such as opium and choral, must be 
rigidly avoided; when once administered to the patient, the comfort 
of the attendant is at an end. Chloroform inhalations may be used to 
relieve certain cases of convulsion and contracture. 

Means of combating special symptoms are innumerable and will 
readily suggest themselves to the physician who is fully cognizant of 
the purely psychic nature of the disease. 

As soon as possible hysterically paralyzed patients should be en- 
couraged to walk. 

The disappearance of special symptoms does not mean that the 
disease itself is cured. Remissions and relapses are to be expected in 
such a constitutional disorder. The means of avoiding these were in- 
dicated under the discussion of the prophylaxis of the disease. 

PSYCHONEUROSES THAT ARE RELATED TO SLEEP AND 
TO THE HYSTERICAL STATE. 

There are certain psychoneurotic states about which there is a 
great deal of confusion and much honest difference of opinion. I 
refer to all that class of phenomena which is variously spoken of 
under the head of hypnosis and hypnotism, dreams, somnambulism. 



THE NEURONIC DISEASES I39 

catalepsy, ecstasy, lethargy, etc. Some authors speak of these as dis- 
orders of sleep; others rank them as manifestations of hysteria and 
mental aberration. They are not exactly normal phenomena, of course, 
and yet many regard them as merely disturbances of a normal function, 
sleep. Others look upon them as absolutely abnormal and in that 
sense not to be spoken of as related to sleep at all. According to the 
latter they are phases of hysteria, possibly evidences of a severe, or at 
least positive, psychosis of fundamental origin. 

In my own opinion much of this confusion is quite unnecessary 
and is the direct outgrowth of certain old-time misconceptions in re- 
gard to the nature of mind and in regard to the limitations or exact 
meaning of the words normal and abnormal. I presume there is no 
dispute in regard to the fact that both sleep and hysteria represent a 
mental change associated with and founded upon some physical or 
physiological change in the nervous mechanism. If we start from the 
standpoint of the state of wakefulness as we observe it in the average 
man, then sleep and hysteria are both anything but a state of normal 
wakefulness. The mind, the consciousness, if you please, is more or 
less in abeyance in both states. We speak of sleep, however, as normal 
and of hysteria as abnormal. Justly so, for though the terms normal 
and abnormal are very elastic, they are used not in the sense of repre- 
senting absolutely what is right and what is wrong, for human knowl- 
edge is not definite enough yet for us to assume that critical standpoint, 
but in the sense of representing what occurs in the average or majority 
of people. All animals sleep, therefore that is normal ; only a few 
animals have hysteria, therefore that is abnormal. Such is the logical 
method adopted by both the scientific and unscientific world. Up to 
a certain point it is a correct and safe method. 

There is a glaring weakness, however, in such reasoning when we 
strive to arrive at exact knowledge. Averages and mere numerical pre- 
dominence do not confirm facts. There must be other features to 
establish them as absolutely undeniable. They must be fixed and 
unalterable ; they must always be identical in every detail ; they must 
appear absolutely always the same under the same circumstances ; and 
we must know absolutely everything about those circumstances before 
we can pronounce the law that they are normal or abnormal. 

As so few of these conditions are made to surround many of the 
phenomena which we now call facts, our assertions in regard to the 
normality or abnormality of the latter are only approximately and pre- 
sumptively correct. By striking the average we come as near as we 
can in fulfilling the above conditions and that which seems to approxi- 
mate most nearly to abiding by them we call facts and declare them to 
be normal or abnormal. 

Sleep is such a normal fact; hysteria is such an abnormal fact. 
When we begin to verge away, ever so little, from the average, we at 
once find that our normal and abnormal facts are a little shaky and 
at once seen to be open to variation and exception. All men sleep, 
but how? Some longer, some shorter; some profoundly, some lightly. 
There are degrees of sleep then, and perhaps other characteristics about 
it that are not necessarily exhibited in the average. At once they be- 



I40 THE NEURONIC DISEASES 

come abnormal, these exceptional sleep variations. A man who sleeps 
a whole month or one who does not sleep at all for a month are both 
abnormal because the average man does not do either. But how about 
the sleeping itself, the prolonged abeyance of consciousness — is that 
abnormal? The prolongation of it, of course, is exceptional and 
abnormal, but so far as we can determine the sleep, the mere abeyance 
of the consciousness, is not abnormal. Again, few men have hysteria, 
but those that do have it exhibit also variations and exceptions in their 
manner of revealing it. There may be such a profound yet partial 
abeyance of the mental faculties that the patient for the time being 
seems to be in another world entirely ; on the other hand, the condition 
may amount to only a high degree of egotism or emotionalism, such as 
even so-called normal men exhibit in periods of unwonted excitement. 

There are degrees of hysteria or psychosis, then, and variations 
from the extremes of madness down to the normal manifestations 
of mere excitement. 

Now it begins to be clear why opinions differ as to the normality 
or abnormality of certain mental exhibitions. There is a midground 
which shifts from normal to abnormal according to the reasoning, the 
predilections and the personal equation of the investigator. 

All of these psychoneurotic phenomena then we will grant are 
forms of mentalization, extending from the complete abeyance of it on 
the one hand (temporarily in sleep, permanently in death), to the ex- 
treme riotous and decidedly exceptional exhibition of it temporarily in 
hysteroid conditions, permanently in certain forms of insanity on the 
other hand. 

To avoid all confusion in regard to the middle-ground of the 
psychoses, the terms normal and abnormal had better be dropped. 

These troubles, then, of mentalization, falling between sleep at 
one end of the line and extreme idiocy, dementia and insanity at the 
other, involve the mind and its anatomico-physiological basis as well 
as all its variations and their particular anatomico-physiological bases. 

A definition of mind has been the goal of philosophers of all time. 
Physiological psychology defines it as a function, a compound of the 
interplay of certain well-recognized sensory-motor functions or im- 
pulses. It is therefore not an entity itself, but a mere phenomenon, a 
process, representing the complicated action and interaction of certain 
anatomico-physiological functions upon one another, or all together. 

That is the physio-psychological definition and conception of mind. 
It does not oppose the discussion of any other conception or object in 
the least to metaphysical debates in regard to dualism, in regard to the 
mind being a separate entity apart from brain, or in regard to the 
existence of immateriality or any other such knotty problem. It simply 
doesn't enter that sphere of research, but merely declares that so far 
as it is concerned, cessation of brain function means cessation of mind,, 
partial cessation of brain function or disturbance of it means partial 
cessation or disturbance of mentalization, an abnormal psychosis. 

With this brief attempt at clearing away the confusing factors in 
regard to the physiological meaning of the terms mind and normal,. 



THE NEURONIC DISE VSES 141 

we are in a better position to analyze and understand the psychoneu- 
roses mentioned at the head of the section. 

Sleep is a function which, when performed under what are called 
normal conditions, represents a complete abeyance of all mentalization. 
with complete absence of consciousness. There is no proof for the 
belief held by some that mentalization never ceases, even during- sleep, 
and that we merely are unable to remember when awake what our 
thoughts were doing when we were asleep. The most reliable evidence 
all points to the fact that in healthful sleep the mentalization is abso- 
lutely at a standstill. The mere nutritive and vegetative functions that 
underlie it go on. 

Healthful sleep being a physiological phenomenon, it hardly calls 
for further description here* Like ail physiological functions, how- 
ever, it is sometimes disarranged. 

The disturbances of sleep are many and varied. Dreaming is 
probably the commonest disturbance. In fact, so> common, so near 
to the experience of the average, is dreaming, that the world looks upon 
it as a normal condition, another evidence of the fallacious method 
of arriving at knowledge by identifying that merely which can be 
predicated of the average with normality. 

Dreaming represents an incomplete sleep, a partial cessation of cer- 
tain high neuro-physiological functions, a partial awakening of mind. 
Dreams, of course, are innumerable and in their partial character repre- 
sent all phases of mentalization. In a broad way, however, it may be 
said that the imaginative, creative faculties and the memory are active, 
whereas the volitional and reasoning functions are in a state of in- 
activity. The inhibitory control of the latter over the former is with- 
drawn and thus is accounted for the rapidity, the strangeness and the 
incongruity of the actions in our dreams. Most wonderful combina- 
tions and thoughts and doings arise in this state. They remain uncon- 
nected by the higher psychic forces. They are so marvelous that 
primitive, ignorant and superstitious people look upon them as super- 
natural visitations, as flights of the soul into space, and as telepathic, 
clairvoyant, spiritualistic and prophetic agencies. They are purely 
psychic phenomena, of course, and doubtless depend upon an abnormal 
interplay for the time between the basal anatomico-physiological func- 
tions of the brain. They have their counterpart metaphorically in the 
physical sphere in the spastico-ataxic manifestations of certain diseases 
of the upper motor neurones, which withdraw the inhibitory control of 
these neurones from those seated in the cord below. 

Pavor nocturnus, the night terrors, seen in both adults and children. 
but more especially in the latter, is usually a psychopathic manifesta- 
tion that occurs when sleep is passing, according t<> the experiments of 
Kohlschittter, from its maximum intensity to a lesser degree of depth. 
It is thus a sort of a dream, but occurring in an individual with a neu- 
rasthenic or hysteric tendency it assumes the depressed, distressing. 
psychalgic form which eventuates in fright and terror. 

Nightmare, so-called, is ;i dream state in which the fancy revels in 
the creation of paralytic conditions or in which the volition especially 
is suppressed while the other facilities are partially awake, especially 



142 THE NEURONIC DISEASES 

the apperceptive faculties. Sometimes in these dream states the apper- 
ceptive functions are so far awake that ideas and questions may be 
presented and be taken in by the sleeper. There is not a complete closure 
here of the pathways for afferent impulses. The whole dream and its 
direction may thus be guided by a touch on the body or a sound in the 
room, or a sudden flash of light. The stimulus may be an auto- 
stimulus and come from the body within. Thus are accounted for the 
dreams that are provoked and directed sometimes by an over-loaded 
stomach or a full bowel. 

In all of these states the sleep is abnormal ; the dreaming is an 
abnormality and rests on an abnormal anatomico-physiological basis. It 
is the result of an abnormal interplay between the inpouring and in- 
poured afferent impulses. Some of the mental functions are active,, 
some are inactive. Thus a strange and abnormal mentalization obtains. 

Sometimes these partial mental activities include the emissive or 
motor centers. A psychoneurotic reflex, a sort of low volition, or rather 
ideo-volition, with a reflex, is set up and the individual does things in his 
sleep. Thus we have the somnambulistic phenomena accounted for. 

Hypnotism is nothing but a form of artificial somnambulism. 
Partial abeyance of the mental faculties is the basis of all these exhibi- 
tions. An automatism characterizes them and just as the withdrawal of 
certain mental forces, and the concentration of certain others, causes 
the wonderful ideas that are enacted in the simple dreaming state, so 
the same disproportion between them enables the somnambulist to do 
the remarkable feats that he sometimes does. A sleeper, for instance, 
can walk on the perilous edge of a roof because, unlike one who is 
awake, he is not embarrassed by any observations or thoughts of the 
dangers of his situation. In regard to them and other attendant circum- 
stances his mind is asleep. All that it is taking in are the impulses 
pouring up from his feet or his. hands, his ears or his eyes. In a reflex 
way these impulses pass through the subconscious or lower coordinat- 
ing apparatus and out again to the appropriate muscles. The sleep 
walker is thus a veritable automatic mechanism ; a most delicate one, 
to be sure, but a completely unembarrassed mechanism. 

Automatism is a trait of all animals and is seen in many common 
acts of life. The developmental stage in regard to the intelligence, the 
habits and the mental capacity all determine a man's degree of automa- 
tism. Automatism sometimes gives one credit for heroism. A man 
rushes into danger often because he is a stupid automaton. The old 
adage that fools rush in where angels fear to tread is another way of 
defining automatism in men. What is vulgarly called "nerve" is a semi- 
automatic performance which a higher degree of intelligence would 
forego. 

Habits establish automatism. Most of the common acts of life, 
like walking, speaking, writing, many of the rarer accomplishments, 
like piano playing, tight rope dancing, trapeze swinging, are perform- 
ances practiced as habits until they have become automatic. They are 
the result of a subconscious reflex and during their performance the 
mind, so far as they are concerned, is partially asleep or wholly diverted. 

That somnambulism is but the same sort of automatism is shown 



THE NEURONIC DISEASES I43 

in the fact that the habits of the individual often determine the char- 
acter of the sleep performances. A writer gets up in his sleep and 
writes ; a singer sings ; a mechanic goes to his tools. 

In ordinary somnambulism the stimulus to the mind comes from 
within. It is an auto-automatism. In hypnotism, on the other hand, 
the stimulus comes from without. The suggestions of the hypnotizer 
enter into the partial mentalization of the patient and their origin not 
being recognized by the higher reasoning faculties whicn are asleep, 
they enter into the mental reflex, give it its direction and so cause the 
subject to do what the hypnotizer suggests. 

This is mere artificial somnambulism. It is an abnormal sleep 
phenomenon, an automatism given directly by an external ideo-motor 
suggestion. It is certainly not a normal condition in the sense of being 
an average experience. It is a pure functional disturbance in the 
psychic sphere and so far as it is allowable to speak of functional dis- 
turbances or of the underlying inherited or acquired nervous defect 
upon which such disturbances are usually based, as conditions of dis- 
ease, hypnotism and all its allied phenomena are disease manifestations. 
They resemble hysteria and other psychoses in being abnormal or ex- 
ceptional forms of mentalization. 

Hypnotism is a subject that has been much written upon, and about 
which many divergent views have been expressed. The history of the 
development of the subject is interesting in the extreme, but would not 
be especially pertinent here and would take up too much space. Suffice 
it to say that at the present time it is founded upon suggestioii and all 
of its phenomena are the result of the influence of the suggestions of 
the hypnotizer made to the hypnotized. There is no transference of any 
physical force or influence. The subject acts in response solely to his 
own mental mechanism, but that mental mechanism is given its direc- 
tion of activity by the suggestions offered to the susceptible subject. 

To-day there are two schools whose opinions upon some features 
of hypnosis and hypnotism are somewhat dissimilar. The Nancy 
school, at the head of which is Bernheim, and the founder of which was 
Liebault, does not regard hypnosis as an. abnormal state in the strict 
sense of the word, for it argues that all men are more or less influenced 
by suggestion and it is only a question of degree as to the susceptibility 
of the individual. It declares, therefore, that taking human beings just 
as they come, eighty per cent, of them at least are hypnotizable. 

The Paris school, at the head of which stood Charcot, insists that 
hypnosis is a decidedly pathological phenomenon and that it is allied 
to genuine hysteria. It maintains that only the weak-minded and un- 
balanced, those who tend toward the hysteroi i state, can be hypnotized 
in the legitimate sense of the word. Ah men, of course, they admit. 
are open to suggestion, but hypnotism is something more than mere 
suggestion. It needs a defective organism on the part of the subject 
for its proper revelation. 

It seems to me that the difference between the opinions of these 
two great schools rests upon some fundamentally different ideas apart 
from the subject of which they are the prominent exponents. Their 



144 THE NEURONIC DISEASES 

debate is really around the word disease, or that which may be con- 
sidered normal or abnormal. 

That all men are open to suggestion is a truism insisted upon by 
the Nancy school ; few men have hysteria is the truism uttered by the 
Paris school. Is all suggestion in its influence hysterical, or, on the 
other hand, is hysteria nothing but a form of suggestion? If the two 
schools can be brought to a point where they can answer these ques- 
tions in exactly the same way, their difference, it seems to me, will have 
vanished into thin air. 

The mind is a mobile phenomenon evolved by a very mobile 
anatomico-physiological basis. It is never the same for obvious reasons 
at different times in the same man, and, still more especially, never 
the same in two different individuals. Its mobility and changeability 
vary according to the stimuli that provoke it into existence, and the 
condition of the physical basis upon which those stimuli act. It is 
therefore always more or less susceptible to change under these condi- 
tions. If the stimuli are strong or if the physical basis is unstable, 
just in the same proportion will the susceptibility of the mind be to 
change. This may occur and yet the condition not be regarded as being 
abnormal. There is an indeterminate point, however, beyond which the 
susceptibility does deserve the name of disease. When the instability is 
so great that every form of stimulus, whether from within or from 
without, controls and directs the mental operations, wholly or partially, 
so that the individual seems to have no self-control whatever, the state 
becomes hysteroid, may even become an actual hysteria, may pass into 
a profound form of pure insanity. 

As I have pointed out in the section upon hysteria, this disease is 
one of mental unbalance, a true psychosis, in which a certain form of 
suggestion, egoistic auto-suggestion, plays a prominent role. In hys- 
teria the patient's mental state is a sort of waking somnambulism, if 
I may use the apparent contradiction. One part of the mental mechan- 
ism is out of balance with another part. The inactive part may not 
be asleep or below the normal waking state, but the active part is too 
vigorously awake and in excess of the normal waking state. To use 
metaphors, it is not that one part of the mind is so much paralyzed as it 
is that another part is in a state of spasm. 

This unbalance is so pronounced and so intense that it affects the 
ingoing and outgoing impulses even, and we call the condition a psycho- 
neurosis on account of the marked physical and mental clinical mani- 
festations. If hysteria be thus a psychosis, a mental unbalance of a 
particular sort, it simulates the condition of the unbalanced individual 
' who is swayed by every suggestion that is poured in upon him. 

If hysteria be a disease, as it undoubtedly is, then the mental 
unbalance is a sort of disease, for it is but a mild degree of the same 
thing. 

Psychosis thus admits of degrees and variations, but we have not 
decided as yet upon the exact line where the normal condition ends and 
the abnormal begins. No man's mind is absolutely impermeable to 
changes of stimuli, or in other words suggestion, for it is itself the very 
representative result of those multiple stimuli. When does the yield- 



THE NEURONIC DISEASES I45 

ing to these stimuli become so great that there is no longer self in the 
process ; or when do the stimuli set up such a powerful, overwhelming 
activity in one direction that there is apparent inactivity in another 
direction ? Who can answer ? He that can will point out to us exactly 
the line between what should be called normal and what should be called 
abnormal. Xear that line, extending on either side of it, in the one 
direction toward perfect mentalization and in the other direction toward 
insanity, will be found the weak and the susceptible individuals who 
are hypnotizable. On the one side they will be regarded as normal 
and possibly number seventy or eighty per cent, of the community : 
on the other they will be considered abnormal and will constitute a 
much smaller percentage. At either end of the line will be found the 
individuals who cannot be hypnotized at all, for either they will have 
too stable or too unstable minds. 

The conditions for producing hypnosis are clear enough. There 
must be susceptibility in the subject and there must be forceful self- 
confidence in the hypnotizer. Infants and insane people cannot obvious- 
ly be well influenced. Weak, neuropathic, rather neurasthenic and hys- 
teroid people make the best subjects. Marked hysteria, like insanity 
and dementia, is not readily amenable to hypnotism. The hysterical 
state between the paroxysms is, however, capable of hypnosis. 

Two things are aimed at in hypnotism. First the patient must 
be put to sleep. This is done by getting him to gaze at a bright object, 
a little above his eyes, thus wearying his eye muscles ; by gently stroking 
the brow outwards with the two hands ; and by urging him to keep his 
attention fixed en the thought of going to sleep while the operator, in a 
soft, monotonous tone of voice, keeps commanding "go to sleep, go to 
sleep ; now you are asleep, sleep, sleep, sleep," etc., repeating this, or 
some similar phrase, over and over until the patient is asleep or rather 
in a state of hypnosis. Ofttimes many trials have to be made before 
success is attained. 

If hypnosis is accomplished, suggestions may then be made to the 
patient to do this or that ; or he may be told that this ill or that ache 
is gone, etc. Be sure always to make the suggestion that it will not 
return when he awakes. 

A quick puff of breath or a command to "awake" will be enough 
usually to revive the subject. 

Of course, it goes without saying that only mental symptoms can 
be thus influenced and not very many of them. Imaginary and self- 
suggested ills are the most successfully managed thus . 

Hypnosis may in a particularly weak individual be set up by inter- 
nal stimuli. This is what is called autohypnosis. It is capable of (level- 
ing from habit. Hence since hypnosis is itself an abnormal condition. 
oping from habit. Hence since hypnosis is itself an abnormal condition. 
hvpnotic state, the practice of hypnotism should be interdicted by law 
except when in the hands of physicians, and by them it should be re- 
sorted to only when other means have failed. 

In certain conditions it is a powerful and legitimate therapeutic 
agent, but it has been very much overvaunted. 

Another manifestation of the somnambulic state is the condition 



I46 THE NEURONIC DISEASES 

known as catalepsy. It is closely related to hysteria and is dependent 
upon the overaction of certain mental activities, to the detriment of 
others. It can be sometimes produced artificially by a loud noise, a 
sudden flash of bright light or a fixation of the eyes upon some bril- 
liant object. The patients become statuesque in appearance. Their 
limbs are waxy-Lke so that they can be placed in any position, and they 
will remain there, without signs of exhaustion. All sensation seems 
to be lost, but the special senses are but little affected. The eyes remain 
open and staring. At times the rigidity of the muscles is so great that 
the patient may be placed with only his head and feet resting on chairs 
and considerable weights laid upon his body. 

In lethargy a still higher degree of abnormal abstraction occurs, 
all the senses, general and special, being abolished. These patients 
cannot be reached by suggestion. The eyes are half closed and the 
muscles are relaxed. Percussion of the nerves may still cause some 
muscular contraction, showing that the neuromuscular excitability is 
still present. It is said that this state can also be produced artificially 
by exerting pressure on the eyeballs in particular individuals, or by 
closing the eyes of one already in a state of catalepsy. 

All of these mental states are hysteroid in character and indicate a 
profound psychic unbalance with enormous overaction in some direc- 
tions and corresponding underaction in others. 

What are the physical changes underlying the phenomena we do 
not know, and probably never will know until we are more familiar 
with the normal mechanism of the mind. 

We have now seen that complete, profound sleep, involving all of 
the mental processes, is a normal condition periodically undergone by 
the nervous system. We have also seen that partial sleep, involving 
only a part of the faculties, may occur in such a mild form, dreams, as 
to be regarded as normal, and yet vary up through the many stages of 
somnambulism, natural or artificial, catalepsy and lethargy to apparent 
death. 

We have noted the similarity of all these conditions, especially the 
latter, with the psychospastic and psychoparalytic phenomena of 
hysteria. 

The last disorder of sleep is its entire absence. This is known as 
insomnia. It is a rare condition and is indicative almost of a form of 
insanity. 

Life cannot be maintained longer than about three weeks in the 
absence of all sleep. What is often called insomnia is merely a mild 
and relative form of the trouble. Drowsiness, short naps and mo- 
mentary lapses that practically amount to light sleep, are experienced 
by those who from various diseases declare they are the victims of 
insomnia. 

The treatment of these relative forms of the trouble consists of the 
removal of the cause and the management of the underlying habits and 
disease. In some insane states a prolonged insomnia sometimes oc- 
curs until the patient dies of sheer exhaustion. 

As I have said, it is impossible to live without sleep: it follows 
that every form of unnatural wakefulness, therefore, has some under- 



THE NEURONIC DISEASES I47 

lving, continuous cause. Absolute insomnia does not exist except for a 
few weeks in certain mental and fatal cases of disease. Relative in- 
somnia, which is the common form complained of, is not a causeless 
trouble. In most cases the cause is obvious ; in a few it may be very 
obscure. Every case of insomnia, therefore, should be most exhaustive- 
ly examined for the cause of it before a moment's thought is given to 
its treatment. There is no mere symptom in neurology that has been 
more often managed as a disease per se, and that as a consequence 
has led to more disastrous habits with drugs and other agents than 
sleeplessness. Even physicians themselves have been their own victims 
in this stupendous piece of folly. Chloral taking and the steady use of 
hypnotics shows on the face of it that a symptom is being wrestled with 
while the hidden cause is still going on exercising its deleterious in- 
fluence. It shows also in too many cases that the adviser is too lazv 
or too ignorant to find out and to combat the cause. And, alas ! it 
sometimes terminates in mania and death. 

The common causes of insomnia are easily grouped under certain 
general heads. In the first place, many people inherit an irritable, weak 
and neuropathic constitution which refuses to functionate normally, 
or as the average, healthy constitution functionates. It is prone, there- 
fore, to be wakeful, with or without adequate provocation. These 
cases are the inherited and habit insomnias. They are purely nervous 
in origin. Some of them may show the nervous insufficiency in vaso- 
motor disturbance which is the cause of the cerebral activity and 
wakefulness. Certain heart and vascular troubles can obviously disturb 
the intracranial circulation. Lithaemia, gout, uraemia and other auto- 
toxic and diathetic conditions can irritate and interfere with normal 
functional activity. Fever is a disturber. Simple exhaustion sometimes 
produces irritability that prevents the much-needed sleep. Various 
substances that are ingested are sleep-destroyers at times, such as cof- 
fee, tea, alcohol, etc. One must also think of the intoxications with 
lead and tobacco, the infections like syphilis, malaria, etc. All of these 
conditions must be earnestly searched for in every case. Only as a 
dernier ressort should drugs ever be employed. 

Before turning in hopelessness to drugs, all sorts of dietetic, 
hygienic, hydrotherapeutic, electrotherapeutic and other mechanical 
measures should be tried first. I always urge that after a light supper 
all earnest mental exertion should be stopped. The evening should 
be passed in as indifferent a manner as possible. Quietude on the 
couch, with a minimum of excitement, such as reading, games, conver- 
sation, should be attempted. Occasionally a slow, short walk in the 
open air for a few minutes in the middle of the evening will be helpful. 
Never take a brisk walk just before going to bed. Some cases do 
well to retire in half an hour after coming in from outdoors. Others 
prefer a slight tepid bath and a little light lunch, such as crackers and 
warm milk. One must experiment here. The great desideratum is to 
quiet the nervous apparatus and to avoid every possible vasomotor dis- 
turbance. Music has a quieting effect nn some, irritating on others. A 
monotonous noise, such as dripping water in a neighboring room, has 
sent an insomniac sometimes to sleep. Monotony of thought, such as 



I48 THE NEURONIC DISEASES ' 

counting, humming, listening to dull reading and repeating senseless 
rhymes, may be helpful to some, but to many others I have found such 
measures to be simply exasperating. There are a hundred ways of 
fostering monotony and quiet and sedation. Each one must learn them 
by experimentation. 

If medicines must be resorted to, I give the preference to trional, 
sulphonal and the bromides. Chloral I consider a dangerous drug. 
More habitues are probably produced by chloral than by any other 
remedy. Hyoscyamus, usually in combination with the bromides, has 
often served well. 

Other hypnotics that may be useful to fall back upon are camphor, 
paraldehyde, methane, amylene hydrate, lupulin, chloralamide, small 
quantity of alcohol, cannabis indica, chloralose, ethylene bromide, 
gelsemium, hypnone, scopalamine hydrobromate, snmbul, tetronal, 
musk, asafcetida and valerian. 

The very length of this list suggests that the drug treatment of 
insomnia is at best only a makeshift. In intractable cases, few as they 
are, and where the cause cannot possibly be discovered, the symptom 
must at times be temporarily looked upon as being the disease itself. 

Never use opium or chloral in these cases except in extremity. 
They will surely become habitues. I have more than once heard a 
physician's reputation torn to pieces by one of these drug takers when 
perchance all he did was to write a single prescription for chloral or 
an opiate. Though the emergency may have demanded it at the time, 
the weak-minded patient seized upon the opportunity to begin a drug- 
habit which had finally driven him to seek a neurologist. 

The treatment of insomnia is not an easy matter. It is one of the 
most difficult tasks in medicine. Its general principles only have I here 
indicated. Firmness, tact and a careful study of the trouble as a mere 
symptom and not as a disease will accomplish the best results in the 
end. Temporary measures, such as the quick, injudicious use of 
hypnotics, will be sure to lead to more or less misfortune. 

Cases of prolonged sleep, lasting from a day even to several years, 
belong to the condition of lethargy, or cases in which a facile habit 
has developed of undergoing autohypnosis. 

Probablv the longest so-called sleep on record is the instance re- 
ported by Herbst, of Bremen, of a woman who was in a state of 
lethargy seventeen years. Ingestion of food was normal except that 
it had to be specially prepared for her. There was a semi-conscious 
state, as she moaned and otherwise indicated when she wanted atten- 
tion. 

The "sleeping" and "fasting girls" of the clime museums are 
lethargic hysterics. 

The so-called sleeping sickness, sleeping dropsy, maiadie du som- 
meil, negro lethargy is a parasitic trouble found occurring endemically 
in Africa, chiefly along the West coast, and limited entirely to the 
negro. The trypanosoma gambiense, recovered from the cerebrospinal 
fluid of the victims, with a species of tsetse fly, Glossina palpalis, as 
the intermediate host, is probablv the cause of the trouble. 

No distinctive pathological changes have been found, though in 



THE NEURONIC DISEASES 149 

one instance there were evidences of a subacute leptomeningitis, 
chromatolysis of various degrees in the cells of the ventral cornua of 
the cord and a slight falling out of the nerve fibres (Warrington). 

The prominent symptom of the disease is the prolonged sleep or 
lethargy, more accurately coma, in which the patients waste away 
and die after several weeks or months, always within a year. 

They rarely recover. Treatment seems to be ineffective. 

VERTIGO. 

Vertigo is a symptom and accompanies many diseased conditions. 
It is only worthy of special consideration because it is such a frequent 
symptom and because it occurs sometimes by itself. 

The imperfection of neurological science is glaringly exposed in the 
way we still have to regard in some instances such mere symptoms as 
vertigo, chorea and hydrocephalus, as though they were special disease 
entities. 

Vertigo is a loss of the sense of equilibrium. It may be sub- 
jective or objective. The victim may imagine his environment to be 
stationary while he himself is in a whirling state, or it may seem to him 
that he is stationary while his surroundings are in a condition of 
unnatural movement. Vertiginous sensations involve incoordination 
as well as a loss of equilibrium. 

Some have thought, from the classical experiments of Flourens and 
the phenomena observed in aural vertigo, that the semicircular canals 
were the special and sole organs that subserved the maintenance of 
equilibrium. 

As stated by Edinger, J. Richard Ewald removed the labyrinth 
from both sides of a dog. The result, of course, was a loss of muscular 
tone and of the power to maintain vertical equilibrium. Walking and 
standing were impossible. Note, however, that these troubles were re- 
covered from, "the tracts for tactile and other impressions making up 
for the loss." The ablation of the cortical motor areas was next made, 
with a resulting incoordination and the loss of the power for making 
any regular movements. But even this was slowly recovered from. 
Suspicion being awakened that all movements were dependent now 
solely upon visual control, the mutilated dog was placed in a dark 
room. He immediately fell helpless to the floor. 

If this experiment means anything, it means that coordination and 
the maintenance of equilibrium depend upon several factors, each one 
of which is capable, up to a certain point, of assuming the whole func- 
tion.* The motor areas of the brain, the visual organs and the semi- 
circular canals all pla\ an equally important part. If the semicircular 
canals alone were the organs of equilibrium it is difficult to understand 
how the maintenance of equilibrium could even in the slightest degree 
be reacquired after their removal, in spite of the preservation of the 
tactile and visual senses. 

As I have shown elsewhere, vertigo and the loss of the sense ^\ 
equilibrium are the result of a disturbance in a more extensive sensory- 
motor field than is represented 1>\ the semicircular canals. In view <>! 



J^ " THE NEURONIC DISEASES 

the fact that in certain of the lowest vertebrates (fishes) whose move- 
• ments require the nicest sort of equilibrium there are no semicircular 
canals ; in view of the fact that experimentation has shown, as in the 
dog, that equilibrium may be recovered and maintained after the com- 
plete removal of the labyrinth ; in view of the fact that both anatomy 
and physiology point out that the sense of equilibrium is essentially a 
complicated sensory-motor phenomenon ; and finally, in view of the 
fact that the anatomy of the apparatus of equilibration, of which the 
semicircular canals form only a part, offers a more rational basis for 
its sensory-motor character than does so limited an organ as the semi- 
circular canals alone: I think that we are still justified in asserting 
that the semicircular canals are not alone the organs of equilibration, 
and that the vertigo of Meniere's disease is not due solely to injury of 
the canals, but to the injury done to the elaborate and complicated 
apparatus of equilibration of which the canals constitute a part. 

One object in presenting all this is to show that vertigo, if our 
knowledge of the anatomy of the apparatus of equilibration is at all 
correct, may be produced by irritation of any of its other ramifications, 
as, for instance, in the eye and in the stomach as well as in the ear. 
Hence, it seems to me that Gowers' statement referring to other forms 
of vertigo than aural vertigo is too much of a pure assumption as it 
stands : "It is certain that in the majority of cases in which such 
vertigo has been ascribed to other causes, these have only had an 
exciting influence and the symptom has been essentially due to the effeci 
of unobtrusive labyrinthine disease, bringing the center into an unstable 
condition." 

The study of vertigo is one of the most intricate in medicine, and 
though we are quite familiar with its subjective and objective mani- 
festations, its immediate cause remains yet a profound mystery. The 
maintenance of equilibrium cannot be satisfactorily assigned to any 
single center, though its disturbance may easily depend upon a number 
of distant reflex disturbances. There is a multiplicity of impressions 
constantly pouring in upon the brain through the various avenues of 
sense which must necessarily keep the mind in a state of extreme ten- 
sion, so that the slightest exaggeration one way or the other will result 
in mental confusion and more or less vertigo. We learn instinctively 
how to control and marshal these ever-passing sensations before the 
mind, but if for a time they become too frequent, rapid or sudden, th* 
controlling force of the intellect is weakened and we are confused an J 
overcome by them. Everybody knows how quickly vertigo is estab- 
lished by rapidly revolving mirrors, peculiar whirring sounds, electrical 
sensations upon the skin and such distant irritative conditions as dys- 
pepsia and constipation. 

Physiological psychologists arc agreed now that our knowledge of 
the relationship of things, as well as of space and its dimensions, is the 
result of experience gained from the use of our muscles. The infant 
learns these dimensions by the frequent application of its hands to the 
objects which it sees; and the sight, which is the only other sense 
that reveals to us an extended object, and that never shows us more 



THE NEURONIC DISEASES 151 

than two dimensions at one and the same time, does so entirely through 
the "muscular sense" exercised in the use of the muscles of the eyeball. 

Now when we study the nature of equilibrium we discover that 
it is dependent upon a normal consciousness of the proper relationship 
of things outside of the centers of consciousness. It is not purely 
pyschic, as some have imagined. There is the sensation of a motor 
process in it. Dr. Hughlings Jackson has long insisted upon the im- 
portance of this fact, while Dr. Reynolds wrote as long ago as 1854 
that "the feeling of equilibrium results from the harmony of our differ- 
ent sensations among themselves and with the motor impulse which is 
their combined effect. When any one group of the sensorial impres- 
sions is distorted or removed, the balance is disturbed, and as these 
impressions are themselves the stimuli of muscular action, attempts are 
made for its restoration . . . producing vertiginous or allied move- 
ments." 

The principal factors m the preservation of equilibrium are there- 
fore consciousness and normal sense impressions. A vertiginous im- 
pression reflected through consciousness may end in a complete or in- 
complete motor act. In the latter case there is merely a residual dis- 
turbance of past impressions without a fulfillment of the present 
impulse in complete motion, while in the former the patient is uncon- 
trollably moved in one direction or another. 

If the views of Spitzka and Starr in regard to the sensory paths 
in the medulla be correct, they bear strongly in favor of this sensory- 
motor theory of vertigo. Thus Spitzka concludes that impressions from 
the cochlea reach the cortical centers in the superior temporal gyrus 
by way of the posterior division of the eighth pair of nerves, the 
trapezium of the same side, part of the lemniscus, posterior pair of the 
corpora quadrigemina, external geniculate body and the corona. Ac- 
cording to some observations of Starr, which prove the correctness of 
the views of Flechsig and Von Monakow, the lemniscus tract is asso- 
ciated with the so-called "muscular sense'' and is chiefly distributed to 
the inferior quadrigeminal body. Some phvsiologists think that it is 
even continued up as far as the corona. It is believed that this tract is 
associated with the sense of sight, as well as with the coordination of 
movements. Flourens found that injuries to the corpora quadrigemina 
of one side caused ''forced movements," and that their complete removal 
resulted in incoordination of movement. 

The point which I desire to insist upon is the close relationship 
of all these tracts for sight, hearing and the "muscular sense" in the 
corpora quadrigemina and their more distinct termination in the 
cerebral cortex than in the cerebellum. If vertigo were a kind of en- 
cephalic ataxia, and due simply to disturbed coordination, it might 
readily be attributed to the cerebellum. 

While the function of the cerebellum may be that of coordination 
and the maintenance of "continuous tonic muscular contractions," and 
while as Spitzka tersely remarks, it may be the center where "impres- 
sions of touch and position 'ire associated with those of time and 
space," I find no authority for assuming that it is in any way the cen- 
ter for the institution of movements or the maintenance of these move- 



152 THE NEURONIC DISEASES 

merits in a regular, methodical manner, which, to my mind, is the un- 
derlying phenomenon, objectively or subjectively, of true vertigo. 

Vertigo is something more than simple incoordination, though 
incoordination may enter as one of its principal elements. In vertigo 
there is a disturbance, not merely of the reflex functions, but of the 
higher powers as well. The motor and sensory phenomena of vertigo, 
in typical cases at least, are not mere sequences of abnormal motor and 
sensory impulses, but they are the impulses themselves. 

Simple incoordination manifests itself in irregular unmethodical 
movements and thus shows that it is due to an affection of some sub- 
ordinate regulating center of the brain; true vertigo manifests itself 
in regular methodical movements and thus reveals disease of a higher 
independent center. 

It is a significant fact, when considered in this connection, that the 
vertigo which is so characteristic of cerebellar disease and which is 
identical with the vertigo of Meniere's disea.se, is caused only by lesions 
in the middle lobe, or that part of the cerebellum which is most liable 
to involve the sensory-motor tracts of the medulla; and furthermore, 
that lesions of the lateral lobes not pressing upon or involving the 
middle lobe do not give rise to any known symptoms. 

And it is still more significant that vertigo is not pathognomonic 
of cerebellar disease, for it may be caused by lesions in other parts of 
the brain as well. Even in its coodinating function, it is more than 
probable that the cerebellum, instead of sending out direct coordinating 
impulses to the muscles, merely coordinates the impulses sent down 
from the cerebral centers above. Indeed, as Ranney has said, "it is a 
curious fact that most of the effects of cerebellar lesions are attributable, 
to a greater or less extent, to irritation of the crura." 

According to Goltz, Serres, Cayrade and others, the function of 
equilibrium is profoundly affected by destruction of the corpora 
quadrigemina. The experiments of Ferrier upon monkeys, fishes and 
rabbits, and of McKendrick upon pigeons, revealed the same effects. 
The corpora striata have also been shown by physiological experiment 
to preside over the maintenance of equilibrium, especially after the 
removal of the hemispheres. 

Every indication points to the fact, then, that we must look for 
the center of equilibrium not in one particular part of the brain, but 
in the harmonious action of the various sensory and motor centers one 
upon another. 

Vertigo then being merely a symptom no systematic discussion of 
its etiology and pathology is possible for we would have to discuss all 
the diseases in which vertiginous sensations occur. 

I have already shown the nature and general causation of the phe- 
nomenon and now will mention a few of the more common forms of 
vertigo and their probable etiology. I do this with the special desire 
of forestalling the various views which some promulgate in regard to 
the cause of all vertigos. 

Ocular Vertigo. The eves and the optic nerves constitute a most 
important inlet for afferent impulses. Any disorder in the visual ap- 
paratus must necessarily upset the orderly procession of these impulses 



THE NEURONIC DISEASES 1 53 

both in relation to one another and to those from other sources. Hence 
we find in nearly all diseases, whether functional or organic, that exer- 
cise the slightest influence on the optic apparatus and the function of 
sight, more or less vertiginous sensation. It is a mere repetition then 
to say that muscular insufficiencies, refractive errors, reflex functional 
disturbances, intoxications, brain lesions, are all more or less accom- 
panied by vertigo. 

Aural Vertigo. The same may be said of diseases of the ear that 
was said of those of the eye. One variety of aural vertigo has long 
been dignified with the special name of Meniere's disease. The latter 
term is employed very loosely nowadays and many writers speak of all 
forms of vertigo whether due to internal, middle or external ear abnor- 
malities as types of Meniere's disease. In true Meniere's disease only 
the semicircular canals are affected. At least that is what Meniere 
himself seems to have believed. His second and fourth propositions 
are that certain functional troubles, having their seat in the internal 
auditory apparatus, may give rise to cerebral symptoms such as in- 
tense vertigo, uncertainty of gait, turning to the right or left and fall- 
ing, all of which may be attended with nausea, vomiting and syncope, 
and that all this tends to confirm the belief that the lesion which is the 
cause of these functional troubles is in the semicircular canals. In his 
original paper he describes ten cases, in only one of which was there 
an autopsy. This case, the tenth of the series, had no disease of the 
nervous centers, but the semicircular canals were filled with a "reddish, 
plastic material." It was on the strength of this single observation 
that he declared the canals to be the cause of the cerebral symptoms. 

Aside from the unscientific character of such a hasty generaliza- 
tion, this one case, as Bremner points out, will hardly explain those in 
which the cerebral symptoms come and disappear rapidly. And if the 
hemorrhage into the semicircular canals were the cause of the trouble 
here and in the majority of the apoplectiform cases, as Knapp argues, 
it remains to be shown why the hemorrhage is bilateral, since the aural 
symptoms are so frequently bilateral. 

Both Steiner and Sewall carefully removed the semicircular canals 
from the shark, whose auditory apparatus is practically identical with 
man's, without obtaining any disturbance of movement. The former 
experimenter believes that the loss of equilibrium results from lesions 
of the brain or its membrane, causing alterations of pressure, for he 
has again and again destroyed the canals in sharks, frogs and lizards 
without injuring the brain, and discovered no disturbance in the power 
of equilibration. After careful investigation Bottcher and Baginsky 
have come to the conclusion that the cause of the rotation of the head 
in Flourens' and Goltz's experiments was the injury done to the brain, 
and not merely to the semicircular canals. Bottcher marks the fact that 
the auditory nerve is not bound down at any point between the brain 
and the labyrinth, and that if. one is careful not to pull upon this nerve 
the vertiginous sensations are not awakened by the injury of the semi- 
circular canals. The slightest traction upon the auditory nerve in- 
jures its attachment at the medulla, and s< rise to the symptoms 
described by Flourens, Cyon, and Goltz. fn the experiments of 



154 THE NEURONIC DISEASES 

Bottcher the head, furthermore, did not always rotate in accordance 
with the particular canal injured, as Goltz had formulated. The iden- 
tity of these canals with the cochlea in the embryo, their continuity with 
the epicerebral space through the aquaeductus vestibuli, and their ever- 
shifting relations amongst themselves in the quadrumana,' which go 
about sometimes in the horizontal and sometimes in the erect position, 
argue strongly against the special function of these canals being the 
maintenance of equilibrium. 

In the discussion of my paper upon the same subject before the 
Philadelphia Neurological Society, Nov. 24, 1890, Dr. Dercum re- 
ported some observations he had made of the comparative anatomy of 
the labyrinth for the purpose of securing new light, if possible, upon 
the function of the semicircular canals. He said : "They bear a dis- 
tinct relation to the lateral line organs of fishes, the nerve hills of the 
latter being identical in structure with the maculae acousticae. Just as 
the inclosure of these nerve hills in tubes seems to have for its object 
the gaining of distinctness and definiteness of impression so the in- 
closure of the maculae within the semicircular canals seems to have the 
same object. It is significant that each macula is situated at the end 
of a canal, and this suggests that the canal is a kind of conduit to carry 
off vibrations after they have made their impression on the macula ; and 
further, that if interference of vibration occurs, it occurs at a point 
distant from the macula. Confusion of sound is thus avoided. The in- 
ference from physiological experiment that these structures have for 
their special object the maintenance of equilibrium, has always seemed 
to me open to most serious objection.'' 

It is a well-known fact that many fishes have a utricle and three 
semicircular canals, while some have only one and two canals. 
Amongst the lowest vertebrates the lamprey has a saccule with audi- 
tory hairs and otoliths in communication with two semicircular canals, 
while the myxine or hag has only one canal. Doubtless there are im- 
portant sensory impulses of a special character which pass through 
these organs, but equilibration, due as we have seen to the fusion of a 
vast complex mass of sensations pouring in upon the brain from all 
sides, cannot possibly be the result of merely a single set of impulses 
from such an end-organ as the semicircular canals. The very nature of 
vertigo involves the idea of more or less loss of consciousness, and this 
alone would seem to indicate a higher cause for the trouble than sim- 
ply these canals. 

If it be granted that the pathological cause of this vertigo is to be 
found in the semicircular canals, it is hard to understand how in all 
cases the cochlea or the cochlea branch of the auditory nerve should 
necessarily be affected. Tn Flourens' experiment, the entire removal of 
the canals did not impair the hearing-. So strikme was this fact, that 
Flourens, as well as others, was led to believe that the branch of the 
auditory nerve which supplies the semicircular canals subserves motor 
purposes only. On the other hand, if Gellc's experiments arc to be 
trusted, the cochlea is in no way the source o\ vertiginous impressions. 

Simple continuity of structure will not account for the loss of hear- 
ing when the lesion is a hemorrhage into the canals, and pressure alone 



THE NEURONIC DISEASES 1 55 

will not answer as a cause in all cases of so-called .Meniere's disease. 
In the first place, there is no regular correspondence between the 
amount of deafness and the intensity of the vertigo ; secondly, with 
total loss of hearing in Meniere's disease all known methods of diag- 
nosis prove that the nerve itself, and not merely the internal ear, is 
affected ; thirdly, physiological experiment shows that simple pressure 
does not cause total loss of hearing when no injury is done to the 
cochlea or cochlea branch of the auditory nerve ; and finally, no case 
has ever been reported in which the cochlea was primarily affected 
with consequent involvement of the canals and vertigo, though in blood 
supply and anatomical structure the cochlea and canals are similar. 
Hence, in Meniere's disease, I conclude that the lesion must concern the 
whole labyrinth or lie entirely outside of it. 

It was Dr. Wilks, of England, I think, who held that Meniere's 
disease was a neurosis of the centers of audition and equilibrium, and 
in its paroxysmal form at least was much like migraine with its eye 
-complications. 

While this explanation cannot be adopted for all cases, there is 
little doubt about the central nature of the disease in many of its as- 
pects. Burnett declared that "the neuropathic diathesis is well marked 
in most cases of aural vertigo." The grouping of the symptoms, as 
well as the proximity of the tracts and centers involved, point to the 
encephalic origin of the affection. Especially is this indicated, how- 
ever, by the sensory-motor nature of the vertigo, whatever be the peri- 
pheral source of the disturbance, and its association with the state of 
consciousness. 

Sudden or paroxysmal vertigo, causing the patient to fall some- 
times as in a stroke of apoplexy, followed by nausea and vomiting, 
headache, difficulty of hearing, stubborn tinnitus or even deafness, bilat- 
eral or unilateral, with various other possible accompaniments such 
as facial paresis, nystagmus, constitutes the clinical picture of Meniere's 
disease. 

According to Meniere himself it is due to hemorrhage into the 
semicircular canals. As the syndrome occurs in other ear troubles, and 
in cranial injuries and brain diseases, the semicircular canals may be 
only secondarily and functionally disturbed. 

In most of the cases the nausea and vomiting soon cease, the ver 
tigo passes away in the course of a few weeks or appears only at re- 
mote intervals, while the hearing remains more or less permanently 
damaged. 

The vertigo of the neuroses bears a close similarity to many c 
of Meniere's vertigo. In hysteria, hystero-neurasthenia, epilepsy, un- 
usual and unexpected sounds, sights and other sensory irritations 
arouse a vertiginous condition. The feeling of distress and impulse- to 
leap which many persons 'nave upon high places is a mild form of 
hystero-neurasthenic vertigo. 

Many irritating and destructive diseases of the nasal cavities, of 
the larynx, and elsewhere about the head often provoke vertiginous 
sensations. 

Intoxications, such as those of alcohol, lead, nicotine, caffeine. 



I56 THE NEURONIC DISEASES 

autointoxication from alimentary disorders and intestinal parasites, in- 
fectious states are all prone to manifest among their most prominent 
symptoms nausea and vertigo. In this class probably falls the so- 
called paralytic vertigo which is endemic in the Geneva canton, Switz- 
erland, and which is attributed by Geslier to misasmatic influences. 
The Kubisagara of Japan is probably the same sort of a trouble. 

Anaemia produces the symptom. Malnutrition of the nervous ele- 
ments may provoke the same functional disorders in them sometimes 
as does intoxication. Atheromatous conditions of the arterial walls 
and circulatory disorders, especially sudden changes in the intracranial 
circulation are characterized by attacks of giddiness. 

The climacteric vertigo is probably largely circulatory in origin 
though other factors play a role also. 

Disseminated sclerosis with its apoplectiform seizures is notable 
for its vertigo. A moment's reflection upon the pathology of this affec- 
tion makes clear the raison-d'etre of the vertiginous phenomena. 

Vertigo may even have a psychic origin. It is not uncommon in 
hypochondriac neurasthenia. Oppenheim even goes so far as to assert 
that it is his belief that every one may produce in himself a feeling of 
dizziness by thinking of incoordination and by depicting to himself 
the feeling. 

Prognosis. The hope of recovery from attacks of vertigo is en- 
tirely dependent upon the curability or removal of the pathological state 
out of which it arises. Intoxication and alimentary vertigoes are prac- 
tically all curable. The dizziness that accompanies arteriosclerosis 
very often disappears as the disease progresses. Sometimes that oc- 
curs in other cerebral troubles, though as a rule these vertigos are ex- 
ceedingly persistent. Removable conditions in the nose, eyes, ears or 
alimentary tract may all be expected to carry with them when removed 
the giddiness which forms a part of their symptomatology. 

Meniere's vertigo is very resistant to treatment. It often disap- 
pears leaving behind it disturbance of hearing. 

Treatment. This should always be toward the removal or 
amelioration of the cause or underlying disease. There is no need 
to say that intoxications, infections, reflex irritants, dyscrasiae and 
cachexias of all kinds, and anatomical and functional anomalies, should 
all be corrected and removed as far as possible. It would be a mere 
waste of space to recapitulate here all of the measures for doing this 
when reference to them can be made to the various chapters devoted 
to the diseases with which vertigo is associated. 

The symptomatic treatment of vertigo should only be temporary 
and when all efforts to remove its obvious cause have signally failed. 
Amyl nitrite, nitroglycerin, the bromides, phenacetin, hydrobromate 
of quinine, alkalies, digitalis, strychnia, etc., may be employed when 
the appropriate condition is present. Glyerinophosphates, gold, the 
ferruginous preparations, bichloride of mercury may be thought of 
for their tonic, and alterative effect and be administered for some time 
in small doses. 

The bromides and belladonna have relieved some cases of 
Meniere's vertigo under my care. The treatment with massive doses 



THE NEURONIC DISEASES 1 57 

of quinine, suggested by Charcot, has ignominiously fafled in a num- 
ber of cases in which I tried it. To be sure the vertigo left after the 
use of the alkaloid for several weeks but Meniere's vertigo not infre- 
quently ceases thus without any medication. Charcot recommended 
that the quinine be given up to the point of cinchonism. At first the 
trouble may be made temporarily worse. On account of the danger 
to the hearing, aurists urge great conservatism in the use of quinine. 
If the patient is willing to exchange deafness for the vertigo, Charcot's 
suggestion to puncture the membrana tympani may be put into prac- 
tice. 

Blood-letting is heroic for vertigo but it has done good in some 
cases when intense congestion was present. In other cases sodium 
salicylate or hypodermics of pilocarpine even- other day have relieved 
most distressing attacks. 

After all it must be admitted that the only treatment of this symp- 
tom is the treatment of the malady to which it belongs. All other at- 
temps to relieve it are unscientific, haphazard and usually disappointing. 

NEURASTHENIA. 

If the term disease is to be made to cover all forms of abnormal 
manifestation, then neurasthenia is entitled to be regarded as a dis- 
ease as well as cancer or syphilis. No manifestation has been more 
happily named, for nerve-tire, nerve-exhaustion, nervous inadequacy 
express exactly the essential condition. It is a nerve-tire, however, that 
is abnormal in the sense that it is not immediately recovered from as 
in the temporary nerve-tire that results from a slight over-exhaustion. 
The nerve-inadequacy has fallen below such a point, either by the 
severity of the cause, the prolongation of the trouble, or the peculiar 
susceptibility of the patient, that certain functions within the neurones 
and in those tissues in direct relationship with those neurones are 
affected. As a consequence a more or less definite symptomatology is 
presented. 

The exhaustion is characteristic of the entire nervous system. It is 
a disease of the nervous apparatus in ioto. Though in different pa- 
tients it may manifest itself more prominently through the cerebral, 
spinal or peripheral nervous apparatus according to the peculiar con- 
stitutional and temperamental predilection of the patient, there is no 
good reason for subdividing neurasthenia into cerebrasthenia. myelas- 
thenia, sexual neurasthenia, gastric neurasthenia, etc. One does not 
divide typhoid fever into diarrhoeal, febrile and delirious types be- 
cause individual patients exhibit more prominently enteric, febrile or 
neurotic symptoms. 

The only logical and practical subdivision of neurasthenia is into 
the congenital and acquired forms. The former is a true nervous in- 
adequacy, a defect of prenatal origin, a failure of biological develop- 
ment; the latter is a true nervous exhaustion, a postnatal depreciation, 
a failure of physiological function from depressing influenc 

Etiology. Heredity plays a very important role in the develop- 
ment of neurasthenia. In the congenital types of the disease it is prac- 



I58 THE NEURONIC DISEASES 

tically the sole cause. The patient is born with an unstable and inad- 
equate nervous apparatus which later on reveals its symptoms of irri- 
table weakness not as a result of the trials and struggles of life directly 
but rather because it cannot meet and override, by reason of its inher- 
ent weakness, these trials and struggles which to a normal nervous ap- 
paratus would be as nothing. In these cases the environment is not 
the cause of the trouble but rather the patient's inherited nervous ina- 
bility to accommodate himself to what would be a normal environment. 

These cases are hard, if not impossible, to treat, because every sort 
of social condition provokes the neurasthenic phenomena in their irri- 
table and unaccommodating nervous organism. 

The large majority of the cases of acquired neurasthenia are en- 
dowed by heredity with what is called a neuropathic constitution. They 
have a nervous apparatus which under proper Conditions may never 
reveal any neurasthenic symptoms but which under other conditions 
leads it to break down rapidly and seriously. Unlike the former class 
of individuals, these are merely unstable. With some of them even 
work and strain that would be unfavorable to perfectly normal indi- 
viduals do not produce deleterious effects. 

These are cases that are always neurasthenic until they are placed 
in a position or are given tasks that harmonize with their tastes, their 
training, their mental calibre and their feelings. In the development of 
these neurasthenics their environment is a most important element but 
it has as a co-operating factor the inherited, unstable, unresisting nerv- 
ous organism which is prone to topple over when that environment be- 
comes particularly inharmonious. Many artists are of this class and 
it is among them that the so-called artistic temperament is mostly 
found. Their nervous organization is not exactly abnormal but it is 
so mobile, sensitive and responsive that very slight causes provoke it 
into revealing abnormal symptoms, which if long continued may result 
in a complete nervous breakdown. 

These cases are amenable to treatment but from the very nature 
of things, their management is difficult, taxing and tedious. 

I should say that from eighty to ninety per cent, of the cases of 
typical neurasthenia fall into one or other of the above classes in 
which heredity plays so important a part. 

Among the antecedents we find various nervous troubles, such as 
neurasthenia, hysteria, migraine, epilepsy, melancholia, insanity and 
other neuroses and psychoses. The family taint runs along the nerv- 
ous line. Gout and rheumatism are not infrequent in the ancestry. 
Alcoholism in the parents, excessive use of tobacco, dissipation, over- 
indulgence of the sexual appetite, are all frequently observed in the 
heredity. Severe and prolonged mental strain without a correspond- 
ing or appropriate attention to their physical vigor and functions In 
the parents will result in a neuropathic constitution in the child. The 
same may be said of all forms of monotonous, one-sided activity 
whether mental or physical. These neurasthenics occasionally expose 
their bad inheritance in slight physical stigmata of degeneracy. 

In a word all factors that tend to lower the mental and physical 
health of the parents, tend to confer on the children a nervous consti- 



THE NEURONIC DISEASES 1 59 

tution that is neurasthenic or prone to become neurasthenic upon the 
slightest occasion. 

The purely acquired cases of neurasthenia, cases in which the con- 
stitution was originally strong and the heredity excellent, do occur 
though they are comparatively rare. In such cases only exciting causes 
can be charged with the disease. 

Among the exciting causes of neurasthenia we recognize both the 
mental and the physical. 

Mental causes include continued and exalted emotionalism, exces- 
sive use of the intellect, and all forms of mental strain, especially it 
associated with worry and anxiety. It is a fact, general opinion to 
the contrary notwithstanding, that mere overwork or hard work does 
not result in mental breakdown, if the individual's inheritance is good, 
the work is not disagreeable and his habits as to sleep, rest, nutrition 
and systematic physical exercise are carefully regulated. If properly 
guarded in this way and if properly exercised in regard to all of its 
faculties equally so as to avoid an unbalanced activity, the human brain 
is capable of bearing a greater strain than is ever put upon it by the 
average work of man. It is the worry, the fret and the one-sided 
strain and unsystematic, unwholesome use of the brain ; and not the 
mere amount of the work imposed upon it, that enter chiefly into the 
mental causation of neurasthenia. 

Close to the mental causes are the nervous strains. Usually the 
two go together. Thus sexual irregularities, excessive venery, and 
masturbation frequently develop neurasthenia though at times they are 
but the expression of a neurasthenic irritability. Cause and effect 
here must be carefully differentiated in each individual case. 

Many of the causes of neurasthenia are kept alive by the neuras- 
thenic state, so that a "vicious circle" obtains and must be broken some- 
where. 

Traumatic neurasthenia is usually due to a psychoneurotic shock. 
The same may be said of the prolonged irritation superinduced by the 
many reflex causes that are mentioned in the books. A local nidus 
of disease, a physical defect which disturbs the associated functions, 
or a physiological abnormality of any sort may well be conceived of 
as an exciting cause, acting in a reflex way upon a predisposed neuro- 
pathic apparatus. In this manner eye-strain, pelvic disease, gastro- 
intestinal trouble with associated malnutrition may all provoke and 
prolong an attack of nervous exhaustion. 

Infectious diseases and all forms of toxaemia may act as causes. 
The toxin may act directly upon the neurones so as to diminish their 
nutritive and specific function, or it may act indirectly upon the pri- 
mary assimilation of the alimentary tract and circulatory apparatus. 
Syphilis for instance injures both the functions of nutrition and the 
neurility of the individual neurones. Any of the infectious disea 
as well as intoxication by alcohol, nicotine, lead and arsenic, may thus 
cause neurasthenia. 

Autointoxication can be invoked as a factor, and in close connec- 
tion with it is the enteroptosis and gastroptosis referred to in Glen- 
ard's theorv. 



l60 THE NEURONIC DISEASES 

A severe loss of blood may very obviously produce neurasthenia, 
the blood being the source of the nutrition of the nervous elements. 
Some careful examinations of the blood of neurasthenics by 
Holdam, Smith Lodor and others show that it is almost constantly 
deficient in oxygen carrying capacity. This of course affects the in- 
ternal metabolism and suggests some form of toxaemia as an underly- 
ing cause. 

Finally it must not be forgotten that even severe and prolonged 
physical exercise sometimes terminates in neurasthenia. Many a mild 
neurasthenic is made worse by adopting, under a mistaken idea, a vig- 
orous regimen of outdoor games and indoor gymnastics. The one- 
sidedness of all such measures, apart from the fact that they only add 
more strain to an already strained nervous apparatus, would seem to 
be enough to condemn them for the treatment of neurasthenia. Euro- 
pean trips, incessant golf and tennis playing, long constitutional walks 
may in this way, when undertaken at the wrong time and without ad- 
vice, be a most fruitful cause of severe nervous prostration instead of 
a remedy as was hoped for. 

Pathology and Pathogenesis. As long ago* as 1869 Beard 
stated his conviction that there were definite structural alterations in 
the nervous system in neurasthenia though undetectable with our pres- 
ent means of research. To call the trouble a functional disturbance 
and deny all possibility of change in the functionating structure is an 
illogical contradiction. 

If the term neurasthenia is to include all forms of secondary as 
well as primary nervous disturbance we will have to admit that there 
is more or less truth in all of the theories of the disease based upon 
the many and various extraneural pathological findings. The etiolog- 
ical substrata of the affection will in many cases have to be included 
in its catalogue of pathological contents. Some consideration will have 
to be given then to the cellular vibratory theory of Beard, the spinal 
hyperaemia and anaemia account of Hammond, the dyspeptic malnu- 
trition of Hayem and Winter, the faulty cellular metabolism within 
the sensory tracts of Jewel, the vasomotor irregularities of Dumas, the 
gastrointestinal disarrangements of Leven, the enteroptoses of Glenard, 
the autointoxication theory of Bouchard, the cerebrospinal hypotonia 
of Cheron, and the altered nutrition in nerve elements of Erb and 
others. 

None of these theories and findings are universally applicable or 
sufficiently constant to make them the basis of a true pathology or 
pathogenesis. 

In simple primary neurasthenia there are no discoverable perma- 
nent pathological alterations in any of the internal organs of the body. 
We are forced to conclude, therefore, that the entire pathology of neu- 
rasthenia as a disease is to be found in the molecular and chemical 
changes, brought about by various causes, within the nervous elements, 
the neurones themselves. 

To C. F. Hodge is due much credit for revealing the changes 
which the neurones undergo as the result of prolonged exercise and 
stimulation. Basing his conclusions upon a series of experiments upon 



THE NEURONIC DISEASES l6l 

the lower animals, he affirms that the cell-nuclei are invariably shrunk- 
en, displaced within the cell and bounded by an irregular, jagged edge. 
They lose their open and reticulated appearance and become darker 
upon staining. There was observed a regular quantitative relation be- 
tween the strength of the stimulus and the amount of nuclear shrink- 
age. The nucleolus in some instances contained granules, which 
moved slowly about and were extruded into the nucleus. The move- 
ments of the nucleoli had every appearance of being amoeboid. After 
they had become somewhat broken up they were rapidly dissolved. 
Under the same conditions the size of the entire cell was diminished 
and its power of absorbing stains was greatly lessened. Vacuolation 
appeared within the cell protoplasm, a proof that the cell substance 
was used up in the action. In this process "the cell tires rapidly at 
first, then more gradually to a condition of fatigue." Vas observed 
that mild stimulation caused a swelling of the cell body while the 
central part of the cell was rendered more or less clear by the move- 
ment of the chromatin bodies toward the periphery. Similar observa- 
tions have been made by Mann who states that it requires prolonged 
and adequate rest to restore these exhausted cells back to their original 
appearance. 

The shrinking of the cell at its nucleus, together with the vacuo- 
lation of its substance, may be made to take place also by the injec- 
tion of various toxic substances into the blood, as has been done with 
absinthe in guinea pigs (Starr). Toxaemia not only affects the cell 
body. In all probability the earliest changes brought about in this 
way in the neurone occur in the delicate protoplasmic endings (Thom- 
son). From experiments made with potassium bromide Wright con- 
cludes that the inhibiting power of this medicament upon intellectual 
and motor processes depends upon its effects upon the ends of the 
protoplasmic processes, while the cell bodies themselves are only made 
to suffer after prolonged exposure to its influence. 

If the blood supply to the nerve cells be diminished or its nutri- 
ent quality be impoverished, changes similar to those just described 
occur with singular constancy in the cells. 

It is a fair conclusion that the same causes, overstimulation, 
toxaemia and malnutrition which with an inherited neuropathic consti- 
tution we see play so important a part in the etiology of neurasthenia, 
produce the same or similar alterations in the nerve cells of the victims 
of this latter disease. 

Symptoms. I am in hearty accord with Dana when he says that 
fifty per cent, of the cases of neurasthenia so-called, may be classed 
under other heads of disease. The term is much abused. 

The symptoms of neurasthenia are not only numerous and varied 
but they never group themselves exactly in the same way in all pa- 
tients. This is not to be wondered at when it is remembered that the 
disease is one involving the whole nervous organism and that its clin- 
ical presentation is modified by the peculiar constitution and tempera- 
ment of the victim. In spite of all this, however, there is a degree of 
uniformity in the clinical picture that makes it worthy of a special 
place in medical nosology. This clinical picture is sufficiently distinct 



1 62 



THE NEURONIC DISEASES 



even to render possible a differential diagnosis of neurasthenia from 
the many other troubles which it often resembles, and with which it 
is frequently associated, though at times it is extremely difficult. 

In a general way it may in the first place be stated that all of the 
symptoms of neurasthenia reveal and depend upon a condition of irri- 
table weakness. Whether in the mental sphere or the nervous, whether 
in the field of sensation or motion, whether vasomotor, secretory or 
trophic, the symptoms that present themselves always represent ab- 
normal fatigue, instability from weakness and diminished power of re- 
sistance, and an utter lack of sustaining force. 

This striking characteristic of the symptomatology of nervous ex- 
haustion is constant and uniform. It is pathognomonic. Analyze 
every manifestation of neurasthenia and if it represents a fatigue 
symptom it points to nervous exhaustion and not to any other neuro- 
sis. It differentiates this disease. 

In all neurasthenics certain symptoms appear with a remarkable 
degree of persistency when one remembers the generalized and ex- 
tensive character of the trouble. Among these may be mentioned a 
peculiar type of headache, and backache, vertigo, insomnia, melan- 
cholia, depression of spirits, bad dreams, cardiac palpitation, nervous 
dyspepsia with constipation and general restlessness and fear of im- 
pending ruin. I will now discuss these and some other indications more 
in detail. 

The patient's mental sphere is always invaded by the disease and 
hence we find that all of his psychic occurrences are depressed. His 
memory is poor, especially for names and the more recent events. His 
power of attention and concentration are annoyingly diminished. When 
reading his mind wanders off upon other subjects though his eyes 
may go on taking in the printed words. He cannot sustain, as he 
used to do, a continuous line of argument. His thoughts at times seem 
to vanish and thus for a moment cause him to lose the thread of his 
discourse. His will power has lost its old vigor; he plans this and 
that but he finds it hard to muster the energy to start his plans. His 
imagination is irritable and active in depicting disagreeable and hor- 
rible scenes. His dreams are all of an unpleasant and depressing char- 
acter. This vicious activity of his imagination is often the cause of 
the partial aboulia. 

The patient imagines all sorts of disasters and unfavorable condi- 
tions that may arise and so dreads to begin any undertaking. His 
judgments are all tinctured with this gloomy, negative view of life. 
He sees everything, as it were, through blue glasses and therefore all 
his acts and thoughts and conversations are suggestive of gloom, pes- 
simism and depression. His whole mind is in a state of psychic pain, 
mild psychalgia. Often the melancholia is so severe that insanity is 
thought of by the patient, his family and family physician. Occasion- 
ally it leads to suicide. 

These cases must be carefully separated from dementia precox, 
attacks of melancholia or manic depressive insanity, and such phrenas- 
thenic conditions as dipsomania, hysteria, obsessions and the exhaustion 
psychoses. 



THE NEURONIC DISEASES 163 

Strange to say, neurasthenics with all their melancholy and de- 
pression are not hopeless of getting well as the hypochondriacs are. I 
make it a rule to question all of them, and gloomy as they may say 
they feel at times, they almost invariably declare they believe they will 
get well if the proper line of treatment can but be hit upon. I almost 
regard this in itself as a valuable sign of true neurasthenia. 

The feeling of dread which these patients have is usually indefinite 
and unaccountable. Often, however, it assumes the definite form of 
a mild phobia. 

The phobias of neurasthenia are innumerable so that only a few 
of them need be named by way of illustration. Agoraphobia (fear of 
crossing a large open square), potamophobia (fear of crossing a run- 
ning stream), claustrophobia (fear of being alone in a narrow place), 
astrophobia (fear of storms), pantophobia (fear of everything) are a 
few of the special varieties. It is unnecessary to dignify these phobias 
as special "fear neuroses,'' as Hecker, Freud and some others have 
done, for they do not occur alone or without some other neurasthenic 
symptom being present. They are of the nature of an obsession or 
fixed idea which is not an uncommon symptom of neurasthenia. 

I had a neurasthenic lad under my care who saw the body of his 
drowned brother shortly after it was taken out of the water. He was 
so much the victim of potamophobia and fear that he would himself 
drown some day that he never could be induced to cross over water. 
When inveigled into approaching a bridge he would suddenly turn and 
run to his room, lock himself in and suffer from severe trembling and 
fright. He recovered in about a year, the phobia and obsession dying 
out as his other neurasthenic symptoms disappeared. 

A young clergyman under my care was harassed with the fixed 
notion that he was offensive and ridiculous in the eyes of every human 
being he met, though as a matter of fact he was most agreeable and 
much sought after. 

These patients are all mentally irritable. They are oversensitive 
and easily offended ; hence they appear egotistical at times and lead 
a more or less solitary life. Their lack of sustaining power makes 
them often appear changeable, frivolous, weak and inconsistent. 

Nearly every neurasthenic complains sometime of vertigo. This 
is not a continuous symptom, nor is it very severe. It is usually of 
the objective type. The patient feels as if he were stationary, while 
objects are whirling about him. Occasionally in severe cases it is sub- 
jective, the patient feeling as if he himself were the spinning object. It 
is provoked generally by sudden and unexpected movements. Often 
the floor seems as if it were rising up. It is not accompanied by vomit- 
ing often, though it is associated not infrequently with a feeling of 
nausea. It never occurs at night nor when the patient is lying down. 
It is experienced in the morning soon after rising. It is felt when 
the patient ascends high places, stands upon the edge of a precipice or 
looks at rapidly moving objects, such as a passing train. Under these 
conditions it sometimes takes the form of an impulsive desire to jump 
from a high place, to rush in front of the train or attempt a sort of 
bird-like flight. 



164 THE NEURONIC DISEASES 

These vertiginous impulses are occasionally very distressing and I 
have known people to be in constant dread from them of committing 
suicide. It is not at all improbable that some cases of unexplainable 
self-destruction by leaping from high places and plunging into deep 
cataracts may have been vertiginous attacks of this sort. 

Insomnia is a remarkably constant symptom of neurasthenia. The 
patient undoubtedly loses a great deal of sleep, but not as a rule so 
much as he imagines he loses. Trie sleep, such as it is, is broken and 
fitful and more or less disturbed with troubled dreams. Sleep during 
the day is almost impossible, even when the conditions are made par- 
ticularly inviting. The early part of the night may be occupied with 
sleep, but about two or three o'clock in the morning the patient awakens 
and thereafter remains awake until the next night. More rarely the 
patient passes the night in short, cat-like naps. Such sleep does not 
bring refreshment and as a consequence neurasthenics always feel 
tired and reluctant to get up when morning arrives. 

Among the subjective symptoms the sensory phenomena, both 
general and special, hold an important place. As aids to neurological 
diagnosis all subjective symptoms, and especially the sensations, must 
be studied with great care. The value of the patient's statements in 
regard to himself must be weighed with caution. Nevertheless, so 
constant and so uniformly similar are some of these symptoms that we 
cannot but help accepting them as distinct and valuable signs of the 
disease. 

The sensations of neurasthenia are generally of the nature of 
paraesthesia, very rarely hyperesthesia or hyperalgesia, and most rarely 
anaesthesia or analgesia. 

Nearly every neurasthenic complains of some form of pain. 
Headache is the most frequent. Even the headache is not a well-defined 
pain, but rather a form of cephalic paraesthesia. The patient complains 
of the head feeling loaded and full; or it is compressed as in a vise; 
or it seems as if it were covered with a heavy, leaden, tight-fitting skull- 
cap. One patient described it as though there were a thousand strings 
attached to her brain and some one were steadily pulling upon them all 
at the same time. Another corrected me every time I used the word 
headache, for she wanted me to distinctly understand that this distress 
was nothing at all like the distinct and painful headaches which she 
frequently suffered from. 

These neurasthenic headaches vary in severity, though they are 
always more or less present. A close observation of them reveals the 
fact that they exacerbate almost always after some unusual or pro- 
longed exertion. Therefore they usually appear shortly after the pa- 
tient rises in the morning. As the stimulation and distraction of the 
day's duties proceed they seem to partly die out, or at least are not so 
noticeable. But in the latter part of the afternoon, when more or less 
physical and mental exhaustion begins to come on the headache re- 
turns with greater intensity even than it had in the early forenoon. 

No other form of organic or non-organic cephalalgia occurs in ex- 
actly this way or possesses exactly these characteristics; hence the 
headache of neurasthenia is a valuable symptom of the disease. 



THE NEURONIC DISEASES 165 

Backache is another very constant sensory symptom. It also is 
fairly characteristic, at least enough so to aid materially in making a 
differential diagnosis from other affections in which dorsal pains are 
present. The entire spine of the neurasthenic feels sore and tender, 
not more so in one part than in another. Pressure and percussion do 
not specially provoke tender spots nor does the passage along the spine 
of a hot sponge or a piece of ice. The pain seems to be eminently 
subjective, being more like a feeling of heaviness, burning, chilliness 
or aching ; it is of the nature of paresthesia rather than a hyperalgesia. 

Some patients complain of a numbness or stiff feeling in the spine 
and its related muscles. They attribute this feeling often to cold, 
rheumatism, or lumbago. It is usually relieved by the recumbent 
posture. 

The nerves of common sensation are implicated in nervous ex- 
haustion. The patient complains of ill-defined feelings of distress all 
over the body and in the viscera; of pressure, of flashes of cold and 
heat; of ill-defined, fugitive pains here and there. The very indefi- 
niteness and indescribable character of these sensations, their varia- 
bility in intensity and their dependence upon the patient's feelings and 
his condition of weariness are their characteristic attributes. 

There are such pains about the heart, leading to a fear of organic 
heart disease. This fear, with the neurasthenic trait of introspection, 
superinduces palpitation. 

Pains in and about the stomach are frequently referred to. As 
they are not influenced especially by the ingestion of food or associated 
with nausea and vomiting and other signs of organic gastric trouble, 
but are accompanied by nervous dyspepsia and troublesome eructations 
and feelings of distension, their nature is easily determined. 

The cutaneous as well as the visceral paresthesia: are sometimes 
very curious. Formication is common. It seems as if ants or worms 
were crawling under the skin. Pinchings here and there and flea-bites 
are imagined and give much annoyance. More frequently there is a 
feeling of coldness in the hands and feet, which the patient invariably 
attributes to poor circulation. Sometimes this peripheral coldness sud- 
denly alternates with a sense of heat as if hot irons were touching the 
skin. 

Among the visceral paresthesia? are such feelings as rectal con- 
striction and paralysis. I have seen some ludicrous cases of this. 
Pruritus ani is in most cases a cutaneous paresthesia of neurasthenic 
origin. 

The bladder may seem to be overdistended, obliging the patient to 
get up unnecessarily often to empty it at night. 

These visceral paresthesia?, when associated with morbid fear, 
sometimes give rise to most amusing situations and lead the neuras- 
thenic in his ignorance to suggest very humorous anatomical and 
physiological explanations. 

One told me once she knew she was losing her mind because she 
could actually feel her brain slowly but steadily softening. 

Patients have insisted that they had a tape-worm, that their lungs 



1 66 THE NEURONIC DISEASES 

were entirely rotted away, that their wombs were misplaced or their 
testicles were shrunken. 

Such patients go the rounds of the physicians' offices and too often, 
alas ! find men who treat them for this or that local ailment so long 
as their money holds out. 

Cutaneous and visceral hyperesthesia is not infrequently met with. 
Simple increase of sensitiveness, without special perversion, may be 
neurasthenic in origin ; it is frequently, however, a sign of organic 
disease. Care must be exercised when making a differential diagnosis 
in the study of sensations that show a simple increase. 

In neurasthenia hyperesthesia is revealed by the patient's abnormal 
sensitiveness to cold and heat, the distress caused by the pressure of his 
clothing. The ill-defined internal sensations associated with the viscera 
are undoubtedly due sometimes to hyperesthesia. 

It is a very rare thing for the victims of true neurasthenia to com- 
plain of hyperesthesia or anesthesia; such sensory feelings belong 
more to hysteria and organic diseases. As hysteria and neurasthenia 
are so often combined in the same individual, the anaesthesia is more 
apt to be a symptom of the former. Nevertheless I have seen cases of 
pure neurasthenia of a profound type in which objective signs of a 
localized hypaesthesia (never anesthesia) were complained of. In 
these cases examination with the faradic brush seemed to show that 
there was not a real loss of sense, at least to an}- marked degree. 

The symptoms dependent upon involvement of the special senses 
are among the most important in neurasthenia because they are so 
uniformly present. Tinnitus aurinm, ringing, buzzing, whistling 
sounds in one or both ears are very common. Frequently the left ear 
is the seat of the trouble and at times it is so annoying that the patient 
declares it will set her crazy. In spite of removal of cerumen and local 
treatment for chronic otitis, which these patients so often insist upon, 
the annoyance continues. Aural hypersensitiveness, on account of 
which the patient starts at every little noise, is rather a psychic trouble 
than an auditory nerve weakness. 

Visual disturbances are represented by spots flying before the 
eyes, so-called musce volitantes, by swimming and vibrating and blur- 
ring of the printed page during reading. The eyes tire easily and 
water freely. Before a glare of bright light they may even pain sharp- 
ly. Vision itself may remain normal ; in fact, it may even be ex- 
ceptionally keen. 

Taste and smell are rarely if ever affected. I have seen a hyper- 
sensitiveness of these senses which was probably a mental or psychic 
symptom. 

The motor symptoms of neurasthenia are of minor importance as 
compared with the mental and sensory symptoms, but they are oi 
value on account of their objective character. They include chiefly 
weakness, tremor, rapid exhaustion and fatigue. The patient never 
puts forth his entire strength when he attempts to perform a muscular 
movement. He shows a marked disinclination and thus in part reveals 
the psychic nature of his trouble. Sometimes, on the other hand, he 
exerts considerable force, but it soon relaxes. 



THE NEURONIC DISEASES 167 

This weakness of muscular action in neurasthenia never advances 
to the point of actual paralysis. In fact, it bears no similarity to or- 
ganic paresis. It is generalized throughout the entire muscular ap- 
paratus and is unaccompanied by atrophy or electrical reactions. 

Muscular overaction or true spasm never occurs in neurasthenia 
in the common acceptation of the term. The tremors and twitchings 
are not so much of the nature of spasms as they are of perversion and 
irritability of normal muscular contraction. Blepharospasm, or twitch- 
ing in the outer corners of the eyelids, is common. It is in part a 
sensory disturbance and in part a fine fibrillary tremor, myokymia. 

Tremor is a frequent symptom and usually consists of rapid vibra- 
tory movements of narrow excursion. Mental excitement and active 
movements in general are accompanied by this tremor. The patient 
says his hands shake when he writes, his head trembles, or his lips 
or his knees, when he becomes unusually excited. Fibrillary tremor 
in the muscles of the leg is often a most distressing symptom. It may 
attack any of the muscles of the body. Many people have cramps in 
the calves of their legs, especially when they are suffering from night- 
mare, but such cramps are not specially indicative of neurasthenia. 

Closely related to the sensory and motor symptoms is the state of 
the reflexes. As a rule the deep reflexes are exaggerated, both those 
of the leg and those of the arm. A foot clonus is sometimes elicited. 
Oppenheim declares that all other signs of muscular rigidity are absent, 
notwithstanding the statements of Binswanger and others. The 
myotatic irritability as well as the nerve excitability are both increased. 
In the severest forms of emaciation the knee-jerks may be diminished. 
Though largely true, it is not absolutely so, as Oppenheim asserts that 
the absence of the knee-jerks means always and only a symptom vji 
organic disease. I know a woman, perfectly healthy in every respect 
except for a slight nervous dyspepsia, in whom the patella tendon re- 
flexes are completely absent. 

The pupillary reflexes are somewhat exaggerated, though the con- 
dition of the pupils is generally normal. 

The irritable weakness of neurasthenia is revealed symptomatically 
in the vasomotor, secretory and trophic mechanisms also. Flushing 
and a rush of blood to the head are spoken of by nearly all patients. 
This is often associated with the vertiginous feeling of faintness and 
cardiac palpitation. The condition is observable objectively, for the 
skin is suffused with a general redness and its temperature is slightly 
elevated. 

Under the name of erythrophobia has been described a most stub- 
born and troublesome form of morbid fear of blushing. 

As Hartenberg has pointed out, the blushing disease, erythropathy, 
should be distinguished from the vicious neurotic circle set up by the 
fear of blushing, or erythrophobia. Shyness or shame, not related to 
fear, causes the flushing. This is a well-defined and frequent phenome- 
non. When fear is added to it, the two emotions influence and react 
upon each other. Blushing creates the fear of blushing and the fear 
creates the blushing. The latter becomes a writable obsession. 

The vasomotor disturbance mav even be so great as to cause 



l68 THE NEURONIC DISEASES 

wheals, as in urticaria factitia. I had a highly emotional young man, a 
professional musician with a high order of poetic temperament, once 
under my care, who almost nightly, as soon as the irritation and warmth 
of the bedclothes encompassed him, suffered from a form of neuras- 
thenic hives. Redness, local oedema and itching were marked. At first 
I thought it was a case of angioneurotic oedema. He fully recovered 
under the treatment for neurasthenia after a number of months. 

Certain special functions are so frequently affected in neurasthenia 
that they have come to occupy a place of considerable prominence in 
its symptomatology. I refer especially to the alimentary, circulatory 
and sexual functions. These troubles are largely subjective in char- 
acter and yet are not without certain objective features. 

Nervous dyspepsia in the broad sense of the term is practically 
always present. The patient complains of not being able to digest his 
food. It often seems to lie in his stomach like a heavy weight. His 
appetite is capricious ; usually it borders well upon anorexia or the 
entire want of appetite. The taste for certain articles of food may be 
changed. There is a craving for stimulants, like tea, coffee and alcohol. 
Shortly after taking the food there is a feeling of distension and fre- 
quently an annoying eructation of gas. Pyrosis or heartburn with water 
brash then follows. Finally this passes into a feeling of rawness and 
irritation in the stomach, with which is associated the old gnawing, 
empty feeling so unlike normal hunger. Nausea is not common and 
vomiting still less so. Persistent thirst and dryness of the mouth are 
common, especially at times of special nervous excitement. It is 
strange that there is not more deterioration of the physical health with 
all these gastric troubles! To be sure, the patients do lose flesh from 
a failure to eat, but the anorexia is the result of the dread of these 
vague sensations of gastric distress coming on, and even in the severest 
cases, wherein there may be vomiting, suffocation, cardiac palpitation 
and meteorism, it is out o>f all proportion to the actual loss in the 
physical condition. The slightly coated tongue, the eructations and the 
frequent hyperacidity add objective confirmation to the patient's un- 
doubted distress. 

Constipation is almost universal, depending upon peristaltic torpor 
and muscular atony. 

Borborygmi and rumbling in the bowels are frequent. 

Occasionally there may be attacks of temporary diarrhoea and in 
some cases there is a constant tendency to diarrhoea, which must be 
guarded against by the avoidance of every sort of emotional excite- 
ment. Scybalous fecal and mucous masses appear in the stools. 

In very rare cases these symptoms lead to a high degree of ema- 
ciation. This emaciation with pallor and loss of strength can be initiat- 
ed by the nervous dyspepsia and continued insomnia. Nevertheless it 
is a fact that a large number of neurasthenics do not suffer from bad 
general nutrition. Some of the greatest sufferers I have seen have 
been people who were outwardly the very picture of health. 

Palpitation of the heart is a symptom very commonly complained 
of. To a certain extent it is subjective in character and is associated 
with feelings of suffocation and precordial pain which may shoot down 



THE NEURONIC DISEASES 169 

the arm. I have noticed that a fear of organic heart disease has often 
been the only thing- that sent these patients forth for medical advice. 
The so-called "tobacco heart'' is a good example of a neurasthenic heart 
It is subject to tachycardia, every wave of psychic activity causing it to 
vary in its rhythm, Intermittency of the beat is not uncommon. 
Allorhythmia and arrhythmia and even bradycardia have all been at- 
tributed to neurasthenia. Anaemic and systolic murmurs may be heard, 
but they are not sufficiently common to make them very valuable as 
signs. Vascular murmurs are spoken of. It is claimed by Gerhardt 
that more than one-half of those who had consulted him for palpitation 
of the heart had some functional disorder of this organ and not valvular 
disease. 

As a result of all these cardiac manifestations a special form of 
neurasthenia — neurasthenia cordis — has been, somewhat arbitrarily, 
established. 

Attempts have been made to locate the trouble in the sympathetic 
nerve or in the vagus, but without any very satisfactory results. For 
the present the irritable and weakened nervous apparatus is enough 
to account for the irregularity of action in an organ so directly under 
the influence of the nervous apparatus as the heart is. 

In the sexual sphere neurasthenia reveals itself in various ways. 
In regard to some of these manifestations it is a difficult matter ro 
determine always the proper relationship as to cause and effect. There 
is no good reason for segregating the sexual symptoms into a special 
form of disease and calling it sexual neurasthenia. The other mani- 
festations of the defective nervous system may be less noticeable on ac- 
count of the prominence of the sexual aberrations, but they will always 
be found if carefully sought for. In congenital neurasthenia there are 
weaknesses and perversions in the sexual sphere that show themselves 
early and are difficult to overcome. Masturbation is sometimes an early 
evidence of the nervous instability and irritability in both the mental 
and physical constitution of the congenital neurasthenic. Indeed Op- 
penheim makes the assertion, and I am inclined to agree with him, 
that the tendency to masturbate can be inherited. The habit once 
established, and ever increased as it always is, puts a strain upon the 
nervous mechanism and reacts upon the patient's mind through fear, 
shame and other depressing mental processes in such a way that the 
neurasthenia out of which the habit originally grew is all the more 
developed. Thus the vicious circle is again established, just as it is 
in the gastric and other special troubles. 

Sometimes these congenital neurasthenics, whether addicted to 
the habit of masturbation or not, are chagrined to find themselves im- 
potent. Usually this is psychic in origin and is due to local irritability. 
Such individuals find that they have their erections, emissions, nocturnal 
pollutions and even the orgasm, all more or less associated with what 
seems to be a normal sexual desire, but under peculiar and abnormal 
conditions, such as when out in society or under the strain of prolonged 
work, or of intense emotion. When they attempt to cohabit normally 
the erection fails to take place, or it is too brief, or ejaculation with 
relaxation occurs before penetration. If the intercourse is accom- 



I70 THE NEURONIC DISEASES 

plished there is such a sudden and complete reversal of the feelings 
from pleasure to disgust that the act becomes one to be avoided rather 
than indulged in. All of this still more depresses the patient and in- 
creases his nervous weakness and irritability. 

Many of the cases of sexual perversion are probably congenital 
neurasthenics. Sadism, Masochism, fetichism, pederasty and all 
forms of abnormal modes of cohabitation may in some instances be due 
to the neurasthenic congenital twist of the mind ; in other words, the 
result of a distinct psychosis : or they may be due to the efforts of a 
congenital neurasthenic to gratify his passion in some way, since he 
is deprived, by reason of his abnormal irritability, of gratifying it in 
the normal way. These abnormal excitations all increase the original 
trouble and the patient becomes still more neurasthenic. 

Spermatorrhoea, prostatorrhcea and all forms of seminal emission 
may be the result of a congenital or acquired neurasthenic weakness. 
Many patients have such discharges every time they defecate. Often 
the urine contains some spermatozoids. All of this worries and cha- 
grins and acts as the real depressing agent and causes the nervous ex- 
haustion more than does the physical effect of the seminal loss. Fiir- 
bringer speaks of an onanistic neurosis and Krafft-Ebing makes the 
attempt of dividing sexual neurasthenia into the three stages, a genital 
local neurosis, a lumbar or spinal neurosis and a general cerebro- 
spinal neurasthenia. This, it seems to me, is an unwarranted and con- 
fusing refinement of classification. The sexual phenomena are but 
one phase of a general cerebrospinal neurasthenia. The prominence of 
the sexual manifestations is due to many factors, such as the con- 
genital or acquired nature of the neurasthenia, the mental characteris- 
tics of the patient, the particular conditions and environment in which 
he lives. The sexual symptoms are distinctly psychoneurotic in origin 
and are dependent upon both general and local influences. They are 
always in part both symptomatic and causative of neurasthenia and 
therefore enter into the constitution of a vicious circle. The recogni- 
tion of this fact has an important bearing upon the treatment of the 
cases in which the sexual features seem to be so prominent. 

The condition of the urine in neurasthenia is not pathognomonic. 
As a rule it is more or less condensed and reveals variable evidences of 
a defective metabolism. The daily amount, as well as the specific 
gravity, is apt to be somewhat below normal. An excess of phosphoric 
and oxalic acid is frequent, but not characteristic, as is too often as- 
sumed. Indican in pathological quantity occasionally occurs and the 
relation of uric acid to the urea varies from I to 40, or 1 to 30, instead 
of from 1 to 45, or 1 to 60, as in normal urine. A transitory glycosuria 
is occasionally met with. Less frequently a temporary albuminuria 
without casts or other signs of renal disease is seen. 

There is no alteration of temperature in neurasthenia, though of 
course vasomotor disturbances may modify the local heat. 

Hypericin) sis is common enough to make it a valuable symptom 
when taken in conjunction with others. Sometimes, however, the skin 
is dry. 

Alopecia and. according to Beard, a tendency to an early decay 



THE NEURONIC DISEASES 171 

of the teeth are to be noted among the trophic general disturbances. 
I have seen oedema as a hystero-neurasthenic symptom 

In spite of the frequent anaemia and loss of weight in many neuras- 
thenics, their blood is not found to be markedly abnormal. The cor- 
puscular richness may be up to the normal and, according to Hosslin, 
there is a healthy amount of haemoglobin. 

A thoughtful consideration of the entire symptomatology of neu- 
rasthenia, I think, will convince any one that it is a disease of the whole 
nervous apparatus. Confusion in the mind of the practitioner may 
result from the fact that all of the symptoms do not stand out with 
equal prominence in every case. In fact, each neurasthenic is a law 
unto himself in regard to the outward expression of his nervous ex- 
haustion. If his inclinations and previous mode of life have been 
intellectual his psychic symptoms will be the more obtrusive ; if he has 
been a mere physical laborer his symptoms of physical weakness will 
"be the more prominent ; if his environment and education have been 
immoral his sexual and other moral delinquencies will give the prevail- 
ing tone to the picture. In all of the cases, however, other manifesta- 
tions will be discovered upon careful examination and thus show that 
the predominant symptoms are but a part of a general symptom-group. 

It is this symptom-group that we must always search for, because 
it possesses certain more or less uniform and persistent characteristics 
that justify the establishment of neurasthenia as a specific entity. The 
subjective characteristics of this symptom-group are the more con- 
stant and regular ones and include the insomnia, bad dreams, melan- 
cholia, vertigo, headache and other pains, paresthesia?, gastric, cardiac 
and sexual symptoms, general weakness and irritability. 

The objective traits of the group are second only to the subjective 
in prominence and constancy. They are sometimes coequal to them 
in value as additional signs whereon to base a diagnosis. They include 
increase of tendon reflexes, cardiac, vasomotor and secretory disturb- 
ances, tremor, increase of muscle and nerve excitability and the general 
history of mental and physical irritability. 

Diagnosis. — The diagnosis of neurasthenia is usually easy ; at 
times it is extremely difficult. It is the safest plan to always diagnose 
it by exclusion, because it so often simulates other affections and not 
infrequently is a part of the clinical manifestation of distinct organic 
disease. For example, the cardiac symptoms at times resemble those 
of various heart diseases; and again in the earliest appearances of syph- 
ilis of the central nervous system the clinical picture is very frequently 
that of simple neurasthenia. 

Much assistance is afforded the diagnostician when endeavoring to 
determine whether a symptom is neurasthenic or not by remembering 
that a neurasthenic symptom is always the expression of an irritable 
weakness; is one of a number of similar symptoms; is variable and 
changeable both as to location and time of appearance; and is a per- 
version of the normal function rather than a mere increase or diminu- 
tion of it. For example, in neurasthenia the sensory phenomena run 
more to bizarre and variable paresthesia? rather than to actual anaesthe- 
sia or hyperesthesia ; psychic and cerebral disturbances assume the 



172 THE NEURONIC DISEASES 

character of melancholy rather than true melancholia, of vertigo of 
psychic origin rather than true organic cerebellar vertigo or ataxia; 
the motor weaknesses are the result of volitional inertia or absence 
of psychic initiative rather than the expression of a true neuromuscular 
paralysis, paresis or spasm. 

Neurasthenia should never be diagnosed upon too small a number 
of symptoms or upon a set of symptoms limited to one sphere of 
physiological activity. It may be convenient at times to speak of gas- 
tric, sexual, cerebral, spinal and other forms of neurasthenia in which 
certain symptoms stand forth with special prominence, but it is highly 
injudicious and unsafe to diagnose neurasthenia from such prominent 
symptoms alone. 

The disease is one of the entire nervous apparatus and the tout- 
ensemble of its symptomatology must be more or less discovered before- 
a clear and decisive opinion can be formed. The same may be said of 
the diagnosis of those arbitrarily classified forms of neurasthenia some- 
times spoken of as primary neurasthenia, hystero-neurasthenia, cli- 
macteric neurasthenia, traumatic neurasthenia, anxiety neurosis, an- 
giopathic neurasthenia, neurasthenia gravis. 

Some further points in regard to the diagnosis of neurasthenia 
itself will be brought out in the discussion of its differential diagnosis. 

The disease with which nervous exhaustion is perhaps most fre- 
quently confounded, because some of the symptoms appear so nearly* 
alike in both, and because they both frequently exist in the same patient 
at the same time, is hysteria. Neurasthenics sometimes develop hys- 
teria, and hysterics are nearly always more or less neurasthenic. Never- 
theless, when both affections are present at the same time it is possible 
often to clearly determine which of the symptoms are due to the neu- 
rasthenia and which to the hysteria. 

The etiology of the two diseases has so much in common, as for 
example heredity, environment and education, it is not to be wondered 
at that a certain resemiblance should obtain between the two sets of 
symptoms. On the other hand, the differences between their patho- 
genetic bases — namely, the purely psychic nature of true hysteria and 
the purely physiological and histological nature of neurasthenia — ex- 
plain and emphasize most clearly the differences in the symptoms — 
even the same symptoms — of the two diseases. 

As Wundt, the great exponent of modern physiologic:.! psychol- 
ogy, has shown, mental phenomena are compounds representing inter- 
connections between certain elementary sensations and feelings. Con- 
cepts, judgments, memory, imagination and volition are not actual 
entities with a local habitat in the brain ; they are mere processes,, 
occurrences resulting from the interplay of the psychic elements, sen- 
sations and feelings. The latter are the only psychic phenomena known 
to have a distinct, local, anatomico-physiological basis. This being so, 
it is obvious how the symptoms of a pure psychosis, as, for instance, 
hysteria, should be so changeable, variable and abrupt, and should 
represent more or less faithfully normal physiological activities, but in 
an exaggerated or diminished form rather than in an actual perversion. 
In hysteria, therefore, we observe an irritability with a heightened sug- 



THE NEURONIC DISEASES 1 73 

;gestibility and the individual symptoms assume the character of a 
psychoneural anaesthesia or hyperesthesia, paralysis or spasm, exalted 
imagination or absent volition. The striking peculiarity of these symp- 
toms is their psychoneural distribution, and above all their incom- 
parable changeableness and sudden variability. They are utterly de- 
void of anything like stability and permanency ; they are mere increases 
or diminutions along normal lines ; they are the results of an unin- 
Jierited or overinherited clash of two or more psychic forces represented 
in the elementary psychic sensations and feelings. They are the ex- 
pression of a true psychosis and can only be effectively reached and 
managed through psychic means. 

Neurasthenia, on the other hand, while necessarily revealing itself 
in part through the psychic sphere, is not a true psychosis. It is an 
organic disease, using the term organic in the sense that disturbance of 
function necessarily presupposes disturbances of the nervous elements. 

It does not matter whether our present means of investigation fail 
to reveal to us the nature of the molecular, chemical or other dis- 
turbance, whatever it may be, in the neuroses or not. The fact remains 
that they are altered, else they would have functionated normally. 

The outward expression of this alteration of the elements in the 
neurasthenic state is that of an irritability with inability for sustained 
activity ; in other words, an irritable weakness. 

This organic basis of neurasthenia, about which we know so little 
positively as yet, lends a certain degree of permanency and persistency 
to the symptoms, a more or less definite anatomico-physiological dis- 
tribution to them, and a tendency towards positive aberrations and 
perversions in them, rather than mere exaltations and diminutions of 
normal psychic and sensory-motor activities. One or two brief illus- 
trations will make this clear. Headache is a symptom of both hysteria 
and neurasthenia. In hysteria it is a distinct pain, often in the vertex, 
when it is known as clavus. The pain sense is one of the normal 
psychic elementary senses. In hysteria this normal elementary sense 
is psychically exaggerated. In neurasthenia the headache assumes 
more of the character of a paresthesia. It is described as a pressure, a 
constriction, a pulling, a vise-like cap, but never as a distinct pain. 
Many times I have had neurasthenics stop me when I have used the 
word headache, in referring to their head trouble, saying that they had 
had headaches, but felt sure that this feeling was not like their distinct 
attacks of headache. Again, anesthesia of psychic origin is pel haps 
the typical symptom of hysteria ; no such anesthesia ever occurs in 
even the most profound state of nervous exhaustion. The rare form 
of numbness sometimes complained of by neurasthenics, if examined 
objectively, is seen to be not an anaesthesia at all, but rather a subjective 
form of paresthesia. 

And so on through the whole list of symptoms common to both 
■diseases. A careful consideration of them from the two standpoints 
just described will enable one to determine whether they are hysterical 
or neurasthenic in origin, even when they appear in a patient afflicted 
with both diseases at the same time. 

Hypochondriasis, a mental malady in which the notion n\ dlSi 



174 THE NEURONIC DISEASES 

is persistently and definitely localized by the patient, often resembles 
neurasthenia with anxiety and fixed ideas. The hypochondriac insists 
that he is never going to recover, but, on the other hand, is steadily 
growing worse, while objectively he is seen to be steadily improving. 
The neurasthenic, when asked, always feels that he is going to get 
well if he is only fortunate enough to get the right treatment. 

Hypochondriacs brood over their supposed trouble, but they are 
not wearily depressed or typically melancholic as neurasthenics are. 
Moreover, they do not reveal the weakness, the bodily emaciation, the 
inability to take prolonged exercise and the other sensory, motor and 
vasomotor symptoms of the latter. In a word, hypochondriasis is a 
pure psychosis of a restricted sort ; the somatic and anatomico-physio- 
logical functions are but little disturbed. 

The form of insanity commonly known as melancholia is some- 
times hard to differentiate from the melancholy of neurasthenia. In 
the former there is a strikingly persistent insomnia, a severe bodily 
emaciation, great restlessness, a high degree of causeless emotionalism,, 
hallucinations and delusions, and a tendency toward suicide. 

Melancholia is a pure psychosis with secondary physical mani- 
festations ; it is subject to abrupt changes in its symptomatology, es- 
pecially outbursts of mania. The face often shows an insane expres- 
sion and the acts of the patient, if closely watched, reveal a mental 
derangement. 

In melancholia the psychic predominance of the clinical picture is 
emphasized ; in neurasthenia the psychic depression is merely a part 
of a symptomatology that includes an irritability and weakness of the 
entire nervous apparatus, motor, sensory, vasomotor and sympathetic. 
And yet it must be frankly admitted that there are cases of melancholia 
and neurasthenia that lie on the borderland between the two diseases 
and in part actually overlap. These are the cases that give the real 
trouble in diagnosis. 

It should not be forgotten that a melancholia patient may at the 
same time be the victim of a neurasthenia and vice versa. Time and 
close observation alone can solve the true nature of some of these 
cases. 

Many gross organic diseases depress the patient into a state of 
neurasthenia, especially in their incipient stages. Among such diseases 
may be mentioned syphilis of the central nervous system, multiple 
cerebrospinal sclerosis, the parasyphilitic diseases, locomotor ataxia 
and dementia paralytica, cerebral tumor or abscess, and certain forms 
of toxaemia involving the nervous apparatus and resulting in gross 
lesions later on. The differential diagnosis of these will be discussed 
under the head of the respective diseases. 

Myasthenia gravis occasionally suggests neurasthenia. The weak- 
ness is here, however, more decidedly neural. It verges more upon a 
distinct paralysis. The bulbar prominence of the manifestations, their 
remarkable remissions, and the absence of sensory and psychic mani- 
festations are to be noted. 

Neurasthenic symptoms may be provoked in a reflex way In 
gross lesions and disease outside of the nervous system. The constant 



THE NEURONIC DISEASES 175 

and severe pain of cancer, for instance ; the ceaseless distress caused by 
an inflamed uterus or bladder ; the anxiety and worry incident to a 
knowledge of organic heart disease may so strain the patient's nervous 
inhibition and self-control as to wear it out functionally and thus set 
up a condition of neurasthenia. 

The value of this observation lies in the direction of urging the 
examiner to spare no pains in searching for all such possible extraneural 
sources of the neurosis. The mere removal of this extraneural trouble 
may not cause the neurasthenia to immediately vanish, for the latter 
has grown into a distinct entity and needs attention solely on its own 
account. 

Neurasthenia is a slow on-coming disease. Even those cases which 
seem to develop suddenly or rapidly after some violent mental shock 
or physical traumatism do not at first exhibit the typical neurasthenia 
that they do later on. 

Sometimes the disease steadily progresses for a number of months 
or years and after reaching a degree of moderate severity remains sta- 
tionary. In all this long period there may be remissions and exacerba- 
tions of the trouble, due to various influences acting upon the patient, 
but there is scarcely ever any absolute return to health unless there is 
a more or less complete change of habits and environment. 

Exceptionally there are instances of neurasthenia gravis which run 
a very rapid course, and in spite of everything sooner or later die of 
inanition and complete exhaustion. 

Prognosis. — The prognosis of neurasthenia is generally favorable. 
It is never a fatal disease per se, though, as Oppenheim, Thoma, Regis, 
Frsenkel and others point out, it may through continual fear and emo- 
tion set up incessant acceleration of the heart's action until an organic 
disorder may result or favor the early development of atheroma of the 
heart and blood vessels, which ultimately may be the cause of death. 
When a neurasthenic worries himself into committing suicide the 
mental condition is probably the expression of a pure psychosis. 

Every case of uncomplicated neurasthenia is amenable to treat- 
ment, and under proper conditions most cases get well. This is par- 
ticularly true of the acute acquired cases. It is even true of the chronic 
cases. The congenital cases, of course, are only partially amenable 
to treatment. Medicine cannot recreate an inherited neuropathic con- 
stitution, but it can do a great deal in preventing and overcoming the 
acute outbreak of the disease in such constitutions. 

The character of the heredity, the patient's station in life and 
means for accepting what may prove to be an expensive method of 
cure, and the absence of all signs of other mental and physical disease 
obviously determine the prognosis. Given certain conditions, some of 
the most brilliant results in neurology are obtained in the cure of neu- 
rasthenia. Complete recovery from the most distressing condition- 
often obtained and gratefully appreciated. This is shown by the fact 
that such patients, knowing their neuropathic tendency, guard them- 
selves, when once they have recovered, and often live to a long and 
happy old age. 



I76 THE NEURONIC DISEASES 

Treatment. The successful treatment of neurasthenia depends 
upon several conditions. 

In the first place there must be a clear comprehension of the na- 
ture of the disease and of its underlying physical basis. In other words 
a clear diagnosis must be made, not merely of the patient's condition in 
general, but of the individual symptoms as well. For example a 
psychic symptom may be due to nerve-cell malnutrition (neurasthenic) 
or to disturbed psychic processes (hysteric). To attempt to combat 
it always in the same way will undoubtedly lead to frequent failure. 
The paraesthesiae of neurasthenia whether cerebral or neural in origin 
are quite different from the psychic anaesthesias and hyperesthesias of 
hysteria. 

In neurasthenia there is an anatomico-physiological derangement 
either within or without the nervous system dependent upon malnu- 
trition, toxaemia, exhaustion or reflex irritation. In the treatment of 
neurasthenia, therefore, the center of attack must be made against one 
or more of these factors. Psychic treatment is of no avail except in 
those cases in which there are hysterical tendencies. 

In the second place, the successful management of neurasthenia 
demands the absolute -confidence and ready acquiescence of the patient, 
on the one hand, and the highest degree of tactfulness, authority and 
wisdom of the physician upon the other. Failure to obtain a cure not 
infrequently results from the non-fulfillment of one or both of these 
conditions. From a want of confidence and obstinacy the patient fol- 
lows directions in a half-hearted manner, or delights in combating 
everything that is done or suggested, or listens too readily to all sorts 
of counsel from neighbors and friends and religious cranks. The result 
is obvious. 

The physician sometimes offends from want of tact, or he attributes 
to hysteria, a pure psychosis, symptoms that are neurasthenic and 
anatomico-pathological in origin and adopts a manner and mode of 
treatment that quite insults the patient, such as questioning the veracity 
of her statements; or he is less intellectual, less well informed and 
less cultured than his patient. All of which foretells the inevitable 
result. 

The third and too often the most difficult condition to secure for 
the successful treatment of neurasthenia is one that involves the ques- 
tion of the patient's finances, time and general ability to carry out an 
expensive and prolonged course of treatment. If the same unlimited 
freedom were given the physician treating a case of severe neurasthenia 
that is necessarily given to one who is managing a case of typhoid fever 
or pneumonia, the results would not only be better for neurasthenics, 
but the art and science of medicine would shine more brilliantly in the 
management and cure of the neurosis than it now does in the manage- 
ment and cure of the infection. 

The latter diseases are not cured by medicine, but inevitably run 
their course. The physician merely guards them from certain possible 
complicating conditions. 

In neurasthenia the disease in toto is made to right-about face and 



THE NEURONIC DISEASES I J J 

start upon an upward grade the moment the requisite environment and 
regimen are obtained. 

The failure of medicine to make a better showing in the treatment 
of neurasthenia is largely due to the fact that the patient's financial 
condition, or his inability to leave his business, obliges us to temporize 
and substitute therapeutic measures that are not absolutely the best. 
In all candor and as a matter of personal comfort and professional repu- 
tation, when the charge of such a case is undertaken, the practitioner 
had better tell the truth about the temporizing character of the treat- 
ment. 

There is no routine treatment with established formulae for neu- 
rasthenia. Each case must be managed in accordance with its own 
individual peculiarities. 

Rest and nutrition, both terms being used in the broadest sense, 
are the two words that cover the whole line of treatment for pure 
neurasthenia. Every amusement and exercise, every prescription, must 
be suggested with only those two ideas in view if the case is one of 
pure exhaustion. 

Xot many cases are purely neurasthenic. Certain hysterical mani- 
festations of a mild character usually develop along with the neuras- 
thenic. Therefore many of the therapeutic measures adopted for the 
purpose of procuring more rest and better nutrition of the nervous 
elements may in part be made to subserve the purpose of combating the 
psychic or hysteroid manifestations. In this way we sometimes hit 
two birds with one stone by changing the patient's environment, by pre- 
scribing particular forms of electricity, baths, gymnastics, outdoor 
games, travel, reading and other occupations. Even the medicines and 
dietary ordered may be made to apply to all three demands, rest, nutri- 
tion and psychic change, when all three are combined in the same 
patient. 

The mode and means of combating the third demand will be found 
discussed under the head of hysteria. Here the discussion will be 
limited to the treatment of pure neurasthenia. 

A little ingenuity will enable the practitioner to combine, when 
necessary, the two lines of treatment. 

The first great requisite is rest. Now rest is a broad term and is 
not synonymous with idleness. Ofttimes rest means change of occupa- 
tion, and occasionally a change that may involve greater occupa- 
tion. The rest must be mental and physical. It is rest for a man en- 
grossed in the cares and worries of a great financial undertaking to 
arrange his affairs temporarily so that he can go out into the woods 
and exercise his mind and body close to the heart of nature. It is resl 
for a woman worn out with the physical exertion of caring for a Large 
household of children to lie for a time idle on a bed and have her tin- 
used faculties exercised with a bit of literature, art or music. Et is resl 
for one who has always lived upon lower mental and physical levels to 
climb up the heights of mental and physical mountains where the 
horizon is larger, the skies more expansive and the play of color greater. 

A small back room in a private hospital with a congenial nurse 
an<|a small but well-selected library will, with other accessories, afford 



178 THE NEURONIC DISEASES 

the highest type of rest to one. To another a trip up the Nile, a jaunt 
through Europe, a climb up the peaks of Colorado, a hunting expedi- 
tion through Montana, canoeing in Canada, farming in Illinois or even 
golf, tennis and ball in the park may be genuine rest. 

By not carefully considering the patient's previous mode of life, his 
temperament, his mental and physical demands, mistakes have often 
been made when change of environment has been recommended. A 
European trip has only aggravated some cases of neurasthenia; the 
so-called secluded "rest-cure" in a hospital has brought still more 
misery upon others. 

Rest in the broad sense of change, mental and physical rest, is the 
sine qua non for beginning the treatment of this disease. 

When all things are taken into consideration, perhaps the largest 
number of neurasthenics can obtain the required rest in a private hos- 
pital or home. In this way the expense of travel, the distant separa- 
tion from family and medical adviser, and all the annoyances of de- 
parture and return are obviated. A change of the mental and physical 
atmosphere is thus secured with the least amount of discomfort. There- 
fore most cases of neurasthenia are benefited by a preliminary sojourn 
away from their usual environment in a rest cure sanitarium, home or 
suburban hospital. 

It is assumed, of course, that the management, location and fitting 
of these places are all that they should be, otherwise they are to be 
shunned absolutely. 

To Weir Mitchell a debt of gratitude is owing for the thorough 
manner in which he has studied and outlined the rest cure. Its main 
features consist of more or less seclusion, physical and mental rest and 
forced nutrition. Only a small percentage of cases of neurasthenia, and 
those the more severe ones, need the absolute rest cure carried out in 
all of its details. The general purpose and principles of the treatment 
being kept well in mind, it may be varied by the attendant so as to be 
adapted to the particular needs of the case in hand. The details of 
the treatment may be briefly discussed under the heads of hydrotherapy, 
massage, electricity, diet and medicines. 

In a general way my own method of procedure with a moderately 
severe case of genuine neurasthenia is about as follows : After get- 
ting the patient away from her usual environment into a private hos- 
pital or home, or, if circumstances will not permit otherwise, into the 
home of some friend of the patient, where there is a sunny, well- 
ventilated room fitted up with furniture, pictures, books, flowers, etc., 
that suggest quiet and cheerfulness, I limit, sometimes prohibit, the 
visitation of friends and relatives. 

A willing and refined nurse is selected and requested to continue in 
constant attendance so long as she proves congenial to the patient. 

A few simple games and a list of a dozen or more books selected 
from the essayists, historians, travelers, poets, philosophers, novelists 
and humorists to meet the patient's particular mental requirements are 
recommended. 

For the first week or so very little is done in the way of active 
treatment. The patient is requested to remain on the bed or couch 



THE NEURONIC DISEASES 1 79 

most of the time, to receive a few friends only, to pass the time chat- 
ting and getting acquainted with the nurse and otherwise becoming 
familiar with the new surroundings. During this first week the bowels 
are freely moved daily with calomel or enemata ; the kidneys are 
slightly stimulated with diuretin ; and the diet is quite closely limited 
to milk and broths given in small quantity every hour or two. Sleep is 
enforced by nightly doses of trional or sulphonal. A certain amount of 
psychic suggestion is made upon each visit to the patient, which visits 
are daily or every other day at first. This is to inspire confidence, to 
increase the docility and hopefulness. 

At the end of the first week or ten days of this preliminary treat- 
ment the patient usually recognizes that her physician can dominate 
the disease, for she finds she has slept and that though she is apparently 
more collapsed and ready to take to her bed, she is slightly less irritable 
and melancholy. 

Now the patient is ordered to keep her bed constantly. The calo- 
mel and diuretin are stopped and only the morning enemata continued ; 
the trional and sulphonal are gradually diminished each night; and 
a slightly more generous dietary is allowed. By this time the particu- 
lar requirements of the case are so well revealed that a daily program 
is carefully written out and left with the nurse to execute. The follow- 
ing program suggested by Dr. John K. Mitchell may be taken as an 
illustration : 

7 a. m. Cocoa. 

Cool sponge bath with rough rub and toilet for the day. 

8 a. m. Milk. Breakfast. 

Rest an hour after. 

10 a. m. 8 oz. peptonized milk. 

11 a. m. Massage. 

12 m. Milk or soup. 

Reading aloud by the nurse. 
1 130 p. m. Dinner. 
Rest an hour. 

3 130 p. m. 8 oz. peptonized milk. 

4 p. m. Electricity. 

6 p. m. Supper with milk. 

8 p. m. Reading aloud by nurse one-half hour. 

9 p. m. Light rubbing by nurse with drip sheet. 

8 oz. malt extract with meals, tonic after meals. 
8 oz. peptonized milk with biscuit at bedtime and a glass of 
milk during the night if desired. 

Such a program as the above should never be adopted as a routine 
for all cases. Its chief value is in giving the approximate time fur each 
of the manoeuvres and in forming a skeleton ground plan whereon 
special indications maybe made to meet special requirements. Not the 
least advantage in the use of such a program is the regularity and 
system which it establishes. 

In regard to the dietary suggestions for such a program, it should 
be well understood that a forced nutrition is the desideratum and that 



l8o THE NEURONIC DISEASES 

therefore the only limitations surrounding it are the digestibility and 
nutritious character of the food and the digestive powers of the patient. 
-Sometimes I find it necessary to study closely the patient's idiosyncrasies 
in regard to food ; at other times I urge the use of all kinds of food, in- 
discriminately, that the patient will enjoy most, assisting its digestion, 
when necessary, with the artificial digestants. I get the food into the 
patient, sometimes with the regular meals, sometimes with small, fre- 
quently repeated meals, knowing that in spite of some temporary dis- 
tress, with digestants some assimilation of it will be accomplished. In 
the early dietary milk plays almost the entire role. Even throughout 
the whole six weeks' or two months' course of treatment milk is made 
a staple article. The quantity (two to four quarts a day), mode of 
preparation, frequency of administration and method of rendering it 
continuously palatable are subject to variation. 

The nitrogenous foods are usually considered the best for neuras- 
thenics. Meats, fish, eggs, green vegetables, fruits, with occasionally 
a little tea and coffee, and at all times abundance of water, may be 
taken. 

It is well for this class of patients to avoid such viands as pork, 
stews, hashes, veal and salt meats in general, thin soups, cooked oysters 
and clams, turkey, thick gravies, pickles, pies, pastry and preserves 
and all made dishes. Howbeit as nervous starvation is so largely at the 
base of nervous exhaustion, I would in some cases even allow some of 
these undesirable articles of food if the patient's idiosyncrasy called 
for them to the exclusion of the more digestible ones. The need of 
nutrition is so great that for the time being a certain amount of gastric 
distress may be risked if thereby more food stuff is accepted by the 
patient. 

Stomachic tonics, acids and digestants can do much towards aiding 
the stomach under these circumstances. 

Hydrotherapy is a most valuable factor in the treatment of neu- 
rasthenia. It should be employed for its tonic rather than its stimulat- 
ing or its psychic effect. Therefore I prefer warm or tepid baths daily, 
either upon rising in the morning or just before the massage in the 
forenoon. The tepid sponge bath in bed every morning, or the drip in 
the evening, may be employed in the early period of the treatment. In 
exceptional cases and sometimes late in the treatment when stimulation 
is indicated I use the cold bath or the cold wet pack. 1 am convinced, 
however, that the vast majority of the cases of neurasthenia are better 
off without such vigorous stimulation, at least until the)' are well along 
in convalescence. 

Whether the water is applied cold or hot, in sprays, douches or 
packs, in full baths, half baths or sitz baths, for a long or short time, 
are details that must be decided by the physician in individual cases. 

Massage, especially for women, is a most grateful form of passive 
exercise. It should not be too vigorous at first, though it may be 
administered daily. Gentle rubbing of the entire body towards the 
heart, sometimes with the use of olive or cocoanut oil, is usually all 
that is necessary. Occasionally pinching, stroking and slapping are 
beneficial. Later on active and passive gymnastics, Swedish movements 



THE NEURONIC DISEASES l8l 

and other forms of medico-mechanical treatment should be systemati- 
cally employed. About this time short walks with the nurse, or rides 
in the open air, may be indulged in, always under the physician's in- 
structions, however. 

Electrotherapy is sometimes abused in the treatment of neuras- 
thenia. It should never be begun too early, say before the second or 
third week in the hospital. It should be used at first rather tentatively, 
and had better be dispensed with entirely if it tires or irritates. Above 
all it should never be used in pure neurasthenia under the notion that 
its good effects are psychic upon the patient. Central galvanization of 
the spine with general faradization of the whole body, the former for 
five minutes and the latter for three-quarters of an hour, in some cases 
produces a marvelously restful feeling and provokes the fine fibrillary 
contraction of the muscles. I never saw any benefit from the use of 
static electricity in pure neurasthenia. High frequency currents, it is 
said, are being used with a certain degree of success. The same is 
claimed for the light-cure. 

Psychotherapy from the very nature of things has some influence 
in the management of neurasthenia, though that influence is infinitely 
less than it is in hysteria. It consists chiefly in the confident and assur- 
ing manner of those who are in attendance upon the patient. 

Medicines are valuable only as adjuvants to the other lines of treat- 
ment. They are chiefly tonics, stomachics, chalybeates, carthartics and 
hypnotics. 

Before speaking of them more in detail I want to protest against 
the too frequent use of stimulants, such as strychnia, alcohol, etc., in 
the early treatment of this disease. To whip up an exhausted and badly 
nourished nervous system is not only illogical, but positively harmful. 
Xot only in patented nervines, but, alas ! too often in the prescriptions 
of intelligent physicians do we find these stimulants when neurasthenia 
is the disease in hand. 

Among the tonics available are small doses of mix vomica, the 
mineral acids, quinine, arsenic, phosphorus and iron. Any preparation 
of these may be employed that is most easily assimilable and that upon 
trial seems to fit the case best. Among the cathartics the salines and 
cascara are the best for continuous use. I always gradually reduce the 
laxatives and depend for a while longer on gradually diminished ene- 
mata. The bromides, sulphonal and trional are the hypnotics of choice, 
though these should only be used early in the treatment and should soon 
be replaced by other means of inviting sleep. 

I deem it unwise to make specific suggestions for the treatment 
of individual symptoms. Besides emphasizing the one-sided conception 
of his trouble already held by the patient, it is apt to cause the attend- 
ants to lose sight of the fact that neurasthenia is a disease of the entire 
nervous apparatus and therefore always needs treatment along general 
lines. This statement applies especially to the treatment of the special 
organs at fault in what is called sexual neurasthenia. 

After the patient leaves the hospital or home it is well for him to 
still keep under the observation of his physician for several weeks 
longer, and above all to avoid returning into the same environment from 



1 82 Tl L1C NEURONIC DISEASES 

which he emerged at the beginning of the treatment. His exercise, diet 
and tonics still need some oversight. Moreover the medical adviser 
can even at this period, when the patient is starting a new sort of a life, 
as it were, offer suggestions, propose restraints and lend encourage- 
ment that may prevent a much-dreaded relapse. During the long course 
of hospital treatment a bond of friendship, closer than a mere profes- 
sional association, has not infrequently sprung up that reveals itself 
when the patient has returned to his normal course of life in a mutual 
confidence which, if properly exercised, will keep the patient from 
ever falling into his old state of distressing invalidism. 

THE TRAUMATIC NEUROSES. 

A few years back the discussion about these troubles was loud 
and heated. To-day it has retired almost wholly into the courtroom 
where it is unfortunately mixed up with damage suits. From the very 
nature of the case it will probably continue to be heard there. 

By a traumatic neurosis is meant the more or less sudden appear- 
ance of abnormal manifestations or symptoms of disease in one who has 
recently passed through a severe accident, railway or other sort, and 
who shows nowhere upon his person any outward sign of physical 
injury. 

It is evident that a condition such as this definition would cover 
opens the way for simulation, fraud and malingering. The heat of the 
debate in the past was undoubtedly fanned to an exalted degree by the 
differences of opinion as to whether all such conditions outlined in the 
definition were not simulations. 

In most damage suits it is obviously the interest of the plaintiff 
to establish beyond question the actual reality of his trouble ; whereas 
it is the interest of the defendant to belittle, to prove the unreality of, 
the disease, and even to establish the simulation of it. The first ques- 
tion that always presents itself in regard to these manifestations, there- 
fore, is whether there is any abnormality present or whether the com- 
plainant is not a malingerer. This, of course, involves detective work 
of all sorts, medical as well as lay. 

As cases of trouble following accidents of all kinds continued to 
appear, some in search of damages and some not, it became evident 
that there was actual disease of some sort in them and that the ques- 
tion of malingering should be set aside as an entirely distinct and 
separate one. Can there be a disease from shock or other accident to 
the nervous system and yet no change be found in the tissues of the 
body? 

At last the question was narrowed down to something that scien- 
tifically was worth while answering. It was a question, however, in 
which it seemed there could be honest differences of opinion between 
equally learned and scientific investigators. In other words, it was the 
old, old problem looming up again, but under another guise, as to 
whether disturbance of function can occur without change of structure. 
There were those who answered "No" to this, but there were also those 
who answered "Yes." The reality of the symptoms was granted. 



THE NEURONIC DISEASES 183 

Those who held that disease always meant some discoverable 
change in the tissues at once started to search for such changes in these 
accident cases. In some of them were found effusions, small hem- 
orrhagic foci, minute degenerative areas, meningeal alterations, vascu- 
lar obstructions, etc. On the strength of these few findings and upon 
the character of some of the symptoms, a pathology was erected. 

The influence of the distinguished surgeon, Erichsen, was so great 
that he led the medical world into adopting the view that the trouble 
was a spinal concussion with early molecular changes and secondary 
inflammatory retrogressive processes in the cord. He, Riegler and 
others regarded the condition as essentially organic, as a chronic 
meningomyelitis. Page then took up the subject and in a volume 
argued against Erichsen that no such damage to the cord could possi- 
bly be produced by railway accidents. 

Thus the ball was set a-rolling again and as investigators lined up 
on one side or the other we were edified with a vigorous scientific de- 
bate on the question of the causation of organic and non-organic dis- 
eases. 

But still the cases appeared in which the symptoms were unde- 
niable, but in which the usual signs of organic disease of the cord were 
wanting or were woefully confused. 

The pros and cons having all now been heard, it is to-day prac- 
tically conceded by the authorities of most reliability that the acci- 
dents which are supposed to cause these diseases can and do cause 
them, but that they are not by any means new diseases. The troubles 
which we observe after a severe shock, physical and mental, are of the 
nature of psychoneuroses, though they may have, in the beginning or 
later on, associated with them vascular, meningeal, inflammatory, 
sclerotic and other changes of the brain, spinal cord, nerves and sym- 
pathetic system., 

It is at last recognized that the traumatic nervous troubles are 
of many types. There are, first, the gross surgical cases with their 
fractures, luxations, hemorrhages and compressions of the spinal cord. 

Then there are the true neuroses or psychoneuroses. These arc- 
classified in modern neurology as neurasthenic, hysterical and hypo- 
chondriacal cases. Associated with and sometimes following later on 
these neurotic and psychoneurotic states, there are the hemorrhagic, 
inflammatory and degenerative troubles, or their combinations, in the 
nervous centers. 

The symptomatology of all these is well known, and as I haw 
described them in detail elsewhere they will not be repeated here. A 
traumatic hysteria is the same as any hysteria. A traumatic com- 
pression of the cord needs no further description than what has been 
given it under the head of spinal diseases. Were these traumatic cases 
never to enter court or be mixed up with damage suits, their discus- 
sion as a separate and peculiar set of troubles would disappear from the 
text-books. 

In court, however, there is still much debate as to what is meant 
by a neurosis or a psychoneurosis. Why? Because the law as il 
framed does not concern itself with hypotheses, however thev ma\ seem 



184 THE NEURONIC DISEASES' 

to be well founded ; and those who administer the law are not willing 
or well enough informed in medicine to fully comprehend what is meant 
by a functional disease. The law and the lawyer demand what are 
commonly called physical proofs, evidences that can be actually per- 
ceived by our senses in some way. They do not care, when in court 
at least, if they are told that a large amount of scientific knowledge, 
even the ultimate foundation of all human knowledge, consists of 
inference drawn by a logical deduction from given data. How often 
the witness in a criminal trial is reminded to tell only what he actual-ly 
saw, or what he can swear that he perceived in some way through his 
five senses ! The court does not want to know what he thinks or 
infers. It cares nothing for his forms of reasoning or the logic of his 
argument. It wants from him merely cold, bare facts which it can 
itself behold or could have perceived under the same circumstances. 

This, of course, is the only stand to adopt in legal matters where 
the conflicts of human judgment are brought to a maximum, but it is 
an absurd one to adopt as the ground for the determination of knowl- 
edge. Upon such a basis we could not swear that we knew anything 
positively. Distant planets would have to be brought into court, atoms 
and molecules would have to be magically enlarged, gravitation would 
have to be materialized and weighed, and the vibrations of sound would 
have to be caught and held up for the jury's personal inspection. 

Facts as the law defines them are not the same as facts constantly 
recognized in the scientific world. 

Among these facts which -science accepts but the law does not is 
the one that we can have a functional disturbance in a nervous cell 
and yet not be able to discern it directly by means of any of our five 
senses. Logic can penetrate where the latter fail. It is just as legiti- 
mate to reason from effect back to cause in medicine as it is in astron- 
omy or biology. It is just as legitimate to accept the existence of 
inherent changes in cellular structures of the nervous apparatus when 
the manifestations are constant and uniform, as it is to infer the ex- 
istence of an unseen world when certain constant and uniform perturba- 
tions are observed in the heavens. 

In medicine we have long since advanced to the point where we 
recognize a neurosis or psychoneurosis as an entity, a disease, an abnor- 
mality, due inferentially but logically, to some molecular, chemical or 
nutritional change in the minute nervous elements. 

At the present day it is not incumbent upon the victim of the 
disease to defend that proposition. If the lawyer of the defendant 
wishes to deny it, he has the whole scientific world of medicine and of 
logic to combat, and to permit him to waste the time of the court in 
such a stupendous task is sheer folly. 

At the present day to discuss and deny the reality of the neuroses 
because forsooth we can't minutely define their pathological basis is 
as ludicrous as it would be to discuss and deny sonic forms of insanity 
in which no known pathological changes have yet been observed. 

In a word, then, these court trials should, if properly conducted, 
narrow themselves down to the question of the existence of or simula- 
tion of the neurosis; and in the event that the former is proved to be 



THE NEURONIC DISEASES 1 85 

the case, they should have regard to the relation of the disease to the 
accident as one of cause and effect, and they should determine the 
severity of it as regulating the amount of damages to be awarded. 

In fine, the medico-legal consideration of the traumatic neuroses 
relates at the present day only to the establishment of their presence, 
their etiology and their prognosis. 

Etiology. — One of the questions always brought up in court, in 
fact the question upon which the awarding of damages actually de- 
pends, concerns the general and the particular causes of the neurosis. 

Can a neurosis be produced by shock in an individual previously 
well in every respect, or has the plaintiff's condition been caused solely 
by the admitted accident? 

Another question that also arises is, after granting that the acci- 
dent has served merely to awaken a latent diseased state in the 
plaintiff, how much damages should be awarded for a disease simply 
aroused into activity, in comparison with one actually originated? 

It is admitted by all neurologists at the present day that shock, 
both physical and psychic, can set up an abnormal state in an individual 
sufficient to be termed disease. Lightning strokes, railway collisions, 
concussions can and do produce symptoms which sometimes betray an 
actual physical basis and sometimes do not. In the latter case they 
constitute almost universally the clinical pictures of hysteria and 
hystero-neurasthenia of variable degree. 

YYe call these diseases or symptom-complexes functional for want 
of a better term, but we assume that they are dependent upon molecu- 
lar alterations, involving change of metabolism. 

Severe fright and excitement, mental and physical shocks of all 
kinds have been followed by these troubles when there could have 
been no possible thought of damages. It is perfectly reasonable, there- 
fore, that they might occur when a damage suit is possible, whether it 
be probable or not. 

It can no longer be doubted that a profound psychoneurosis, hys- 
terical or neurasthenic, with all that we include in those disease states, 
may be caused de novo by a severe accident in which there has been 
a severe mental and physical shock. 

Nevertheless it is true that in the majority of cases there has not 
been a state of ideal health before the accident. A shock that would 
produce a pronounced psychoneurosis in a previously healthy indi- 
vidual would be not unlikely to produce a severe physical lesion of some 
sort. Not infrequently such is the case, though it is not often rec 
nized until some weeks after the accident. Embolic and hemorrhagic, 
inflammatory and sclerotic conditions of insidious character are thus 
often initiated and bring in their train a long series of grave mani- 
festations. 

These are the organic ca.-es, and as a rule are the type that occur 
in patients who are caught by the accident when they are in perfect 
physical and mental vigor. 

Very often, however, the victim of the shock lias been the pos- 
sessor of a highly neuropathic constitution. He may even have been 
all his life, or recently, a hysteric or neurasthenic. Hi- nervous ap- 



l86 THE NEURONIC DISEASES 

paratus may have been already on the verge of collapse with alcoholic 
or nicotine poisoning. Meeting with an accident under such circum- 
stances, an unusual psychoneurotic state is suddenly evolved in him 
and he is profoundly prostrated, violently hysterical or pitifully hypo- 
chondriacal, though he may show no physical sign of injury and may 
even not have been as badly shaken up as some others in the accident. 

The latter is, therefore, a definite exciting cause of his trouble, 
though not the primary originator of it. The results may be lasting 
and later on even evidences of physical degenerative conditions may 
make their appearance. 

The relative amount of damages for an accident that originates 
and for one that merely awakens a latent disease state must be decided 
by the legal authorities. 

Symptoms. — There is nothing to be said of the symptoms of these 
neuroses more than what has already been said under the heads of 
hysteria and neurasthenia. 

The detection of malingering depends almost wholly upon symp- 
tomatology. Familiarity with the diseases that are simulated and nat- 
ural shrewdness alone will enable the examiner to detect a fraud. To 
lay down rules of procedure would be absurd. Each case must be 
studied by itself. The whole clinical picture must be taken into view as 
well as the various manifestations in detail. 

Most simulators are dishonest and fraudulent. A hysteric may 
be an incorrigible simulator and yet not be dishonest or fraudulent. 
The examiner must be careful to differentiate the two. One of his 
most difficult tasks, if the case goes into court, will be to convince the 
jury that there is a difference between the hysterical and the fraudulent 
simulator. It is a fact that the laity still look upon hysteria, with its 
high degree of susceptibility to suggestion, as a sort of a make-believe 
on the part of the patient, that gives strength to the defendant's side 
in the courtroom. If a case is hysterical I urge against all litigation. 
A prompt settlement, though small, will be better than to run the 
risk of trying to explain, in the presence of an opposing lawyer, to 
the average panel of layman, what is meant by hysteria and to prove to 
them that it is an actual disease as much as typhoid fever or pneu- 
monia. The task is herculean and even though heavy damages be 
really deserved, the chances are strong that the verdict will be against 
the plaintiff. 

A very good principle to remember in detecting malingering is 
that it is safer for the malingerer to imitate an organic disease than to 
imitate a neurosis, but that it is easier to diagnose a simulated neurosis 
than to diagnose a simulated organic trouble. The reason of this is 
obvious. The neuroses are so much more changeable in their symp- 
toms and have so many more of them than the organic diseases, that 
the chances of inattention on the part of the malingerer are better in 
the former than in the latter. A local paralysis or anaesthesia such as 
we observe in an organic disease can be imitated by a shrewd criminal. 
His attention being confined to so limited a phenomenon, he cannot be 
thrown off his guard by the tests of the examiner. On the other hand, 
scarcely a simulator is so well posted on disease as to be able to present 



THE NEURONIC DISEASES 1 8/ 

a complete and typical picture of a neurosis. He either overacts or 
underacts his part. 

One of the shrewdest simulations that I was ever asked to unmask 
was that of a woman who for years had been representing herself as 
an epileptic. She had clearly studied the disease well from the books. 
Several physicians who had seen her in her fits had pronounced her 
-epileptic. The family history was neuropathic and there had been a 
trauma. In all details she acted her part to perfection. When, how-* 
-ever, the entire history and total picture of the case were brought into 
the light of scrutiny it was obvious enough that the case was not one of 
typical epilepsy. It was not hysterical, nor was it organic. I pro- 
nounced it one of simulation and the later results proved the correct- 
ness of my suspicion. 

Another case that I saw was one of genuine hysteria in which 
imitation had played such a strong role that in the absence of certain 
stigmata of hysteria some of my colleagues thought it was one of pure 
simulation. The total picture of the case formed the basis of my 
■opinion. 

I recently saw in consultation a traumatic hysteria in a man who 
could not move his left arm, could not hear with his left ear and was 
afflicted with complete aphonia. A stroke of lightning had hurled him 
across the room and he was examined about a week later. No organic 
lesion would have given the peculiar complexus of symptoms that he 
presented. Simulation was excluded by the rapid action of the pupils 
to light, with sluggish action to accommodation, and by the entire 
early and late history of the case. 

Simulators who attempt to imitate the neuroses do not render the 
picture changeable enough. They adopt a type of the disease and 
then give its manifestations such a permanency and a uniformity as 
belongs only to organic disease. 

Of course, electricity, a psychic shock, etherization and the state 
of the pupils will serve when in doubt as invaluable aids in differen- 
tiating organic from functional disease and distinguishing either from 
pure malingering. 

Prognosis. — the prognosis of the traumatic neuroses is always an 
important question in court. Much is said on the side of the defense 
about the rapid recoveries that occur after the payment of the damages. 
The insinuation, of course, is that deception has been practiced. Thai 
is undoubtedly the case sometimes. However, there is something to be 
said in favor even of those who thus recover after damages and yet are 
not simulators. It is a fact that the recovering of a large award and 
the satisfaction of having won one's case is a powerful stimulant. A 
neurosis is a functional depression, a continuous autosuggestion in some 
cases. Let such a case be given an experience that would make almost 
any human being glad, honestly glad, and it is nol surprising that 
sometimes it takes a turn and recovers. Psychotherapy is a potent 
agent when administered by a court as much as when administered by 
a physician in the hospital. 

As a matter of fact, however, there are numerous cases "I trau- 
matic neurosis that do not recover immediately or at any time after 



l88 THE NEURONIC DISEASES 

the awarding of suitable damages. Indeed, some of them even get 
worse and not a few develop in the course of a year or so distinct indi- 
cations of serious organic trouble. If the outlook of every case could 
be foretold, the amount of damages to be awarded could be nicely- 
adjusted. Unfortunately there are no safe guides in this respect. 

The traumatic neuroses have a prognosis that is a little worse 
than other forms of neuroses. If there has been a latent neuropathic 
state prior to the accident, the prognosis is rendered very grave. It is 
to be remembered that tabes, dementia paralytica, disseminated sclerosis, 
or spastic paraplegia may have been latent or just beginning to show 
themselves with mild neurasthenic symptoms about the time of the 
accident and that they may be suddenly started into a full and rapid 
progress by the nervous shock of the accident. . 

Aside from such facts as these the prognosis of the traumatic 
trouble follows that of the disease, however it may have originated. 

Treatment. — For treatment, see the sections on hysteria and neu- 
rasthenia. 

EPILEPSY. 

There are some twenty or more synonyms for this disease, so long 
has it been known and so varied have been the explanations of it. Its 
protean manifestations have caused students, from ancient times down 
to the present, to regard it all the way from a divine possession to a 
mere gross anatomical defect. The numerous names of the disease 
in a general way either describe some particular feature in its symp- 
tomatology or suggest an imaginary pathology for it. Falling sickness,, 
fits, apoplexia parva and morbus sacer are among the more striking 
synonyms. Epilepsy, from a Greek root meaning to seize upon, is now 
the recognized title of the disease everywhere. 

It. is easy to say that epilepsy is a condition in which loss of con- 
sciousness with convulsive movements constitutes the principal phe- 
nomenon. Such a definition, however, is inadequate to cover all of the 
various types, many of the aberrant forms and the general mental 
state, while it gives no clue whatever to the underlying pathological 
anatomy. In fact, it is not probable that any short definition of so pro- 
found and varied a malady will ever prove entirely satisfactory. This 
is especially important to remember when the physician is placed upon 
the witness stand in court and pressed to give in a few words a ae- 
scription of the disease. Preceding his testimony with this explanation, 
he may, upon the urgent request of the court, attempt a definition 
somewhat in this wise, remembering all the while that the two cardinal 
features of the clinical ensemble are the sudden loss of consciousness 
and the impairment or loss of motor coordination : Epilepsy is a dis- 
ease of the brain in which paroxysmally and somewhat periodically. 
abruptly and for a brief period of time, the consciousness is wholly or 
partially lost and the muscles are or are not thrown into a condition of 
incoordination with the tonic and clonic convulsive movements. 

There are four well-recognized types of the disease based largely 
upon their symptomatic differences. They are the grand mal, the petit 
null, the partial (Jacksonian) type and the psychic type. 



THE NEURONIC DISEASES 189 

There are certain neuroses that are believed by many to be minor 
manifestations or types of epileptic seizure, such as migraine, certain 
forms of angina pectoris, asthma, nocturnal pollution, gastralgia, 
enteralgia, etc. These will be again referred to under the head of 
epileptic equivalents. 

Status epilepticus is a culmination of the disease, but hardly a 
special type. 

The old division into primary or idiopathic and secondary, organic 
or symptomatic epilepsy is rapidly being obliterated. As our knowl- 
edge increases we are realizing more and more that an organic change 
of some sort in the cortical structures underlies the whole trouble. The 
reason for and the exact nature of this change are the problems still 
awaiting solution. 

Etiology. — The one great truth that stands out beyond all others 
in regard to the causation of epilepsy is that a hereditary taint, more or 
less pronounced, lies behind it. By this I do not mean to say that 
it is a hereditary disease directly, though it is often observed itself in 
the progenitors. Various influences of a neuropathic sort, such as hys- 
teria, migraine, gout, insanity, alcoholism, nervous strain and dissipa- 
tion, syphilis, etc., in the ancestors often reveal themselves in the off- 
spring in the production of epilepsy. In this broad sense, therefore, 
genuine epilepsy is an inherited disease. The predisposing factor in 
its etiology is an inherited, developmental defect in the nervous system 
whereby certain exciting prenatal, natal and postnatal accidents and 
influences cause the cortical neurones to functionate in this abnormal 
manner. A clear heredity can be traced in about one-third of all 
cases. In two-thirds of these the inheritance is direct and of like sort. 
In the remaining cases an indirect heredity is so constantly, though 
ofttimes remotely, discovered that one is almost justified in saying that 
the so-called exciting causes of the disease depend for their potency 
upon the existence of this predisposing element. 

Sometimes where the heredity cannot be elicited clearly from the 
ancestral history, collateral defects and stigmata of degeneracy in other 
children will point it cut. A woman whom I saw recently had never 
had any trouble until she was forty-seven years of age. The family 
history, so far as it was confessed to me, was entirely negative. A sis- 
ter of the patient, however, had cleft palate. Another patient claiming to 
come of a strong and sturdy German stock had had migraine of a most 
seyere type until her first fit, and volunteered the information that her 
sister, as well as herself, were the victims of paroxysmal asthmatic 
attacks. 

Injuries, depressing influences and other factors that ma) affecl 
the growing brain in its early years will cause congenita! defects that 
may express themselves in epileptic seizures. Freud goes so far as 
to say that all epilepsy is due to the developmental defect left in the 
brain by the ordinary lesions of the cerebral palsies of childhood. In 
these cases, of course, what hereditary influence there is must be of an 
indirect sort and probably vascular in character. The traumatic cerebral 
palsies which provoke brain atrophy, sclerosis and other defects out of 
which epilepsy is evolved cannot be spoken of as hereditary. 






190 



TPIE NEURONIC DISEASES 



The disease may declare itself at any age. Partly on account of 
the hereditary and congenital nature of it, three-fourths of the cases- 
begin to show symptoms under twenty years of age. 1 have often 
noticed that an epileptic equivalent, such as migraine, asthma or neu- 
ralgia, will suddenly cease and epileptic seizures take its place at about 
the age of physiological stress, as puberty and the climacteric. It is 
said that nearly fifty per cent of the cases occur in the second decade of 
life, when the awakening of the sexual function and the consequent 
emotional strain are overwhelmingly dominant. 

Partly as predisposing and partly as exciting causes infections and 
toxaemias are particularly significant. The acute infectious fevers of 
childhood, and above all scarlet fever, are responsible for the disease. 
As the cerebral palsies of childhood, from which so many cases of 
epilepsy are to be dated, are also largely due to the acute infectious 
diseases, it is difficult to say whether the epilepsy is the direct result of 
the infection or the secondary result of the brain defect. Pertussis, 
thermic fever, malaria, pneumonia, influenza, diphtheria, measles, 
typhus, typhoid and yellow fever and meningitis have all been credited 
with the disease. Gastro-intestinal disorders with auto-intoxication 
may well be the cause of epilepsy, in view of our modern nutritive 
conception of its pathogenesis. Toxaemia from lead poisoning, exces- 
sive use of tobacco, renal diseases, alcohol and such poisons as cocaine, 
antipyrin, arsenic, physostigmin, chloroform, etc., are to be remembered 
as possible instigators of epileptiform and probably epileptic fits. 

Acquired syphilis may cause epilepsy, though as a rule the seizures 
are indicative of gross lesions of a vascular nature so familiar in 
cerebral lues. Inherited syphilis is undoubtedly responsible for some 
cases. 

Other chronic infectious states that, like syphilis, predispose to the 
disease are rheumatism, scrofula, rickets, gout, severe anaemia, cancer, 
drunkenness of parents at the time of conception, diabetes and possibly 
chorea. 

Dentition in a predisposed child may provoke the disease. In- 
fantile eclampsia may be the beginning of it, a fact which should warn 
us not to make light of infantile convulsions about the period of teeth- 
ing, as is so often done. 

Traumatic epilepsy is usually focal, partial and Jacksonian in type. 
Nevertheless injuries to the head may provoke general epilepsy in 
various ways. Depressed bone, fracture of the inner table, hemorrhage, 
embolic obstruction, degenerative focal encephalitis or meningo-en- 
cephalitis may be the immediate cause of the trouble. 

Mental shock is another factor and has often been the starting 
point of the severest types of the disease. Mental strain, such as pro- 
longed anxiety, worry, grief and exertion in those whose heredity is 
unfavorable, are of the nature of mental traumatic causes. I place here 
the influence of masturbation. Usually this is an evidence, in early 
cases at least, of a neuropathic condition, rather than the cause of it. 
And yet it is clear that the shame, the fear of detection, the periodica} 
excitement and the popular notion that the practice invariably leads 
to insanity, is* of the nature of a mental rather than a physical cause. 



THE NEURONIC DISEASES 191 

The mental power of the old Roman eunuchs shows that the loss of 
the vita sexnalis alone is not the cause of mental deterioration, whereas 
the worry and continued distress that such a condition may provoke 
may be. The horrible results liable to follow masturbation may be 
depicted to a susceptible lad in order to frighten him out of the dis- 
gusting practice, but they ought not to be set down in a scientific work 
to that which is not the real cause of them. Indeed it is questionable, 
in my opinion, whether we do well to play upon the mind of the patient 
in order to coerce him into a better state of morality. The remedy 
may be worse than the disease and by reason of the fright and dread set 
up, a serious mental shock, with all its evil consequences, may be put 
in place of a mere filthy habit. Masturbation, I can well understand, 
may as a secret and vicious practice well provoke in a neuropath 
epileptic seizures. It should be discouraged, therefore, as strenuously 
as possible, without, however, resorting to measures that still more tend 
to disturb and depress the mind. 

Psychic outbursts, ungovernable passion, intense anger and electric 
shocks have formed the starting point of the disease. 

Heart disease is so often found in company with epilepsy that a 
causal relationship is more than a suspicion. Mitral regurgitation was 
the chief cardiac symptom in the 1,070 cases examined by Spratling. 
Some form of heart trouble occurred in 238 of them. 

Reflex epilepsy is still a battle ground of argument and 
opinion. No one believes in the sole causation of the disease 
by peripheral irritation. There must be already present a strong 
predisposition. The unstable equilibrium of the nervous elements must 
be already in existence. That being so, it is both conceivable and dem- 
onstrable that irritating diseases of the internal organs, intestinal para- 
sites, elongated prepuce, laryngeal polyps, carious teeth, eye strain and 
foreign bodies in the ear may provoke the seizures. That is very differ- 
ent, however, from the statement ihat reflex irritations are the cause 
of epilepsy. Putting a stop to the fits is not always curing the epilepsy. 
The removal of these various sources of reflex irritation usually puts 
a stop merely for a time to the seizures. Too often the patient's early 
delight and belief in the cure are transformed into bitter disappoint- 
ment and hopeless indifference at finding that the fits are beginning to 
return again. These may be due to some new source of peripheral 
irritation, and had the exact value of these causes in the production 
of the disease been honestly presented to him, he would be willing to 
continue further treatment instead of basing his resisting obstinacy 
against all further attempts at relief upon the false hopes that were 
raised by the earlier treatment. 

Senile epilepsy has been attributed to an atheromatous condition 
of the blood vessels. It is just as liable to be due to the general senile 
decay and toxaemia from functional insufficiency of the various organs 
as from anything else. 

It is obvious that predisposing causes play the initial role in the 
etiology of epilepsy and that innumerable exciting causes may provoke 
the former into an outward expression. 

The great predisposing causes are heredity, infection and physical 



192 



THE NEURONIC DISEASES 



defects in the brain of a congenital or acquired nature. Cerebral in- 
stability is thus established and constitutes the essential disease. Its 
presence may be discovered and typical epileptic seizures may be pre- 
cipitated, however, only when one or more of a long list of possible 
exciting agents begin to bear upon it. 

Pathology and Pathogenesis. — It would be interesting but un- 
profitable to rehearse all the explanations that have been vouchsafed in 
the past in regard to the pathogenesis of epilepsy. Some of the scien- 
tific accounts of it were no less fanciful and no more founded upon 
actual pathological findings than were the superstitious and religious 
belief that it was clue to some divine or devilish form of possession. 
As in all the great neuroses the, number and variety of hypotheses have 
been in inverse proportion to the number and constancy of the post 
mortem findings. It is only within the last few years that we have 
approached anything like a scientific and well-founded explanation of 
the disease. Much still remains to be discovered, but what we already 
know indicates in the clearest manner along what lines future investi- 
gations should proceed. 

It would be well in discussing the modern explanation of epilepsy 
to always keep a sharp line of demarkation between the actual patho- 
logical findings and the mere surmises and logical deductions that are 
based upon those findings. The former may always be referred to 
with a certain degree of positiveness ; the latter must always be looked 
upon with a certain amount of reserve. 

After noting briefly the actual macroscopical and microscopical 
changes commonly found in epileptics who have died, as well as some 
functional abnormalities frequently observed during life, I will follow 
the recent excellent work of Prout and Clark and indicate the prob- 
able relationship of these various pathological conditions to the cardinal 
symptoms and the disease itself. 

In the gross pathology of the disease we find various more or less 
constant changes in and about the head and the brain. Some of these 
are of the nature of stigmata of degeneracy, some are the residua of old 
diseased conditions, others are the results of arrested development, 
and still others are the direct products of the epileptic seizures. In 
all of this the one fact that stands out with embarrassing prominence 
is that these changes, whether macroscopic or microscopic, cannot 
always be determined as the cause or the result of the disease. 

Almost every sort of lesion of the cerebrospinal axis, its mem- 
branes and their bony envelope, has been seen in epileptics. Deformi- 
ties of the skull, thickenings of the bones, anatomical changes in its 
minute structure are almost constantly observed. They may have 
something to do with the production of the disease, but it is more 
likely that they are the expression of a physical degeneracy of which 
the epilepsy is in part also an expression. The membranes are opaque, 
adherent, thickened in many cases, showing signs of an old inflamma- 
tion, hemorrhage and other vascular troubles. The brain itself not 
infrequent lv shows a partial or general atrophic change with alterations 
in its contour and convolutions. Like the skull, it is often undersized 
and deformed. On the other hand, it may appear perfectly normal. 



THE NEURONIC DISEASES 1 93 

The most frequent findings in it are the remains of the old lesions of an 
infantile cerebral hemiplegia. Spots of softening, old hemorrhagic 
scars, cysts, depressions, porencephalic deficiencies and atrophy may 
be discovered. These are the remains of pre and postnatal cerebral 
hemorrhages, embolism, thrombosis and meningo-encephalitis. Freud, 
as before mentioned, believes that all epileptics owe their disease to the 
lesions that cause the cerebral palsies of childhood, so frequently are 
they found in the post mortem examinations. With or without atrophy, 
the brain is sometimes hardened by an over-production of neurogliar 
tissue, a general gliosis. This is thought by many to be a result and 
not a cause of the fits. 

A sclerosis of the cornu ammonis was at one time dignified by 
Meynert and others as the pathogenetic factor in the disease. It cer- 
tainly occurs frequently, but is only a part of the general cortical 
sclerosis or neurogliosis. 

Cerebral tumors are not commonly the cause of epileptic seizures, 
but that they may be influential in the production of the disease must 
not be lost sight of. They provoke epileptiform rather than epileptic 
seizures. 

So varied, irregular and disconnected are all these gross conditions 
that one can only mention their existence in, without being able to 
postulate definitely their relationship to, the disease proper. They 
may be the outgrowth of the same etiological influences that establish 
the epilepsy, while, on the other hand, they may by pressure and other- 
wise so disturb the circulation and nutrition in the brain as to set up 
the epileptic state and habit in the cortical cells. 

There is no question at the present day but that epilepsy is a dis- 
ease of the brain cortex. For this reason I pass by the older theories, 
such as that of Kussmaul and Nothnagel, which places the primary 
trouble in the medulla and pons, where the vasomotor centers are 
located, that send out impulses which cause spasm of the cerebral 
vessels and cortical anaemia. Through its symptomatology and by 
means of experimentation it is settled that the source of the manifesta- 
tions of epilepsy resides in the cortical cell-bodies. Attempts have 
been made to determine the immediate cause and character of these 
cell changes. Here again theory has been rife, while the demonstrable 
proofs have been wanting. 

Among the more notable theories that have been propounded upon 
the slight histological basis of the cortical findings may be noted the 
cerebral gliosis irritative explanation of Fere. Chaslin and Soimner; 
the undemonstrable fine molecular changes in the cells assumed by 
Binswanger, Cowers, Jackson; the autointoxication view and all its 
minute possibilities upheld by Voisin, Agostim, Coloban, Krainsky ; 
and the views of those like Prus, Hering, Redlich, BischofT, Rothman 
and Von Bechterew, who have attempted to localize the origin and 
extension of the fits. 

By the work of all these investigators many isolated and sug- 
gestive facts have been brought to light, in uniting and comparing 
of which certain broad deductions may be made which will lead us t<» a 
fairly definite conception of the modern pathogenesis of the disc 



194 



THE NEURONIC DISEASES 



The examination of the cortex of twenty epileptics who died at 
the Craig Colony in New York warranted Prout and Clark to assert 
that the most striking changes were found in the cells of the second 
cortical layer, cells distinctly sensory in type. This, as well as the 
general symptomatology, favors the view that epilepsy is primarily a 
sensory disease with certain secondary motor disorders. In these cells 
the nucleus was most affected. It was granular, swollen and poorly 
outlined. The nucleolus was often absent, many hundred times more 
so in sections from status epilepticus cases than in sections from normal 
brains. The nucleus being damaged, the cell nutrition is injured, and 
as a result chromatodysis, often spoken of by other investigators as well, 
occurs. The cortex is invaded with leucocytes, especially after status 
and serial fits, which assume the phagocytic property of removing the 
products of the tissue metamorphosis. A neurogliosis accompanies the 
process, filling up the spaces vacated by the wasting cells. 

Upon these histological findings and the chemical changes and 
alteration of secretions noted but not positively established by others 
in the bodies of epileptics, Prout and Clark deduce that epilepsy is a 
cerebral disease attended and followed by profound and diffuse cortical 
degeneration ; that the morbid changes concern chiefly the destruction 
of the nuclei of the cells of the sensory type from which the primary 
departure of the disease originates and often and in the course of 
which a progressive and more or less marked and diffuse gliosis oc- 
curs ; that it is as a disease essentially a sensory phenomenon with a 
secondary motor manifestation ; that its etio-pathology rests with a 
variety of toxic or autotoxic agents not as yet definitely isolated or 
determined; and finally that it is engrafted upon a cortical organic 
cellular anomaly which is induced largely by a faulty heredity, the exact 
anatomic nature of which is not known. 

The two chasms still to be bridged before the circle of our knowl- 
edge of the pathogenesis of epilepsy can be said to be complete are the 
nature of the heredity and the change it produces in the cortical cells 
whereby they become epileptogenous, and the nature and source of the 
toxic agent that provokes these predisposed cells into the actual state 
of disease. 

In regard to the former we know absolutely nothing except what 
is hidden beneath the phrase developmental inadequacy. In regard to 
the latter the work of many investigations upon the blood, the urine, 
the sweat and the secretions of the ductless glands is suggestive and 
worthy of more than a passing notice. There is a hypotoxic state of 
these various fluids of the body in the interparoxysmal periods of the 
disease, a hypertoxic state just before, during and after the fit. Krain- 
sky and Weber attribute the toxicity to carbonate of ammonium, 
Donath to cholin and neurin, Haig to uric acid. 

In this connection it is worthy of note that the disease has been 
attributed to acetone, to leucomaine poisoning and to a diminished alka- 
linity of the blood. 

There is no conclusiveness or uniformity about the autointoxication 
basis of the disease as yet to warrant more than a passing brief mention. 

Symptoms. — The symptomatology of epilepsy may be studied in 



THE NEURONIC DISEASES I95 

an orderly manner from several different standpoints. Types of the 
disease have been constructed out of the predominance of certain symp- 
toms so that there is a marked difference between the clinical account > 
of grand mal, petit mal, status epilepticus, partial or Jacksonian epilepsy, 
psychic epilepsy and the so-called epileptic equivalents. 

A disconnected account of the seizures may be given as though 
they alone constituted the disease, and the patient's condition between 
the attacks be assumed as one of health. 

Emphasis may be laid upon the slim data which we possess in 
regard to the exact etiology and pathology of the disease and the 
clinical description be varied so as to suit the so-called idiopathic or 
primary and secondary or symptomatic cases. 

In my own opinion the best plan upon which to study the outward 
manifestations of epilepsy is to regard all cases as practically the same, 
with the same general etiology, the same pathological basis and the 
same general clinical exhibition. I will regard the disease, when once 
established, as a continuous and more or less persistent one with mere 
exacerbations, as it were, in the seizures. In other words, an epileptic 
is such not because of his fits merely, but because he has a cerebral 
lesion or disorder which reveals itself occasionally by certain violent 
outbursts. The patient is as much of a victim of disease between 
attacks or fits as during them. He is in no sense in perfect health 
until all evidence or possible evidence of the disease is removed per- 
manently and completely. 

I will make no distinction between idiopathic and symptomatic 
epilepsy, for in their essential pathogenesis they are the same ; nor 
between the general and localized forms, for they too are practically 
the same, except for extent of symptomatic distribution. In other 
words, in the following description I will assume that epilepsy is a 
disease, one and uniform, characterized by a more or less orderly series 
of events in »11 cases and with only some slight variations in its clinical 
presentation as the result of some unimportant variations in the extent, 
origin and location of the lesion. I will note these variations, but 
I will not emphasize them as special forms, separate types or distinct 
diseases. Syphilitic meningitis that focalizes itself in the cervical part 
of the cord is not spoken of as a different disease from syphilitic menin- 
gitis that focalizes itself chiefly in the lumbar part of the cord, and yet 
the symptoms of the one are radically more unlike those of the other 
than are the symptoms of the various so-called types of epilepsy from 
one another. 

The essential characteristics of epilepsy are certain premonitorv 
warnings, a fit or sudden exacerbation with peculiar mental and motor 
phenomena, a group of sequelae and a quiescent interval until the next 
exacerbation. This is the uniform series of events that makes up the 
clinical picture. There may be and usually are many variations in the 
details of this picture. 

The premonitory symptoms, for instance, may be of every sort in 
which involvement of the cerebral functions are implicated. They may 
be so slight as to be practically nil. 

The mental disturbance may be profound and accompanied by 



I96 THE NEURONIC DISEASES 

other most violent and appalling demonstrations, while, on the other 
hand, it may be so slight that it alone seems to constitute the entire 
disease. 

The sequelae may be so pronounced that they seem quite like essen- 
tial traits of the disease; but, on the other hand, they may be entirely 
wanting. Sometimes they assume the role of the so-called equivalents. 

Finally the quiescent interval may resemble perfect health or con- 
stitute a mild degree of general physical and mental invalidism or even 
be occupied by an extension of the exacerbation into the serious con- 
dition of status epilepticus. 

So-called symptomatic epilepsy has no place in this description, 
unless it sets up and is accompanied by the form of the disease now 
under consideration. Symptomatic epilepsy due to gross irritative 
lesions is nothing but an epileptiform symptom of the particular disease 
in which it occurs, and should so be referred to under the symptomatol- 
ogy of that disease. 

The first evidence of the disease is always a fit. A person may 
have been born of epileptic parentage with all the predisposing heritage 
of the disease, nay, more, he may actually be the victim of the disease, 
but no decisive evidence of it occur for years or until he is well along 
in middle life. If the fits should be mild and nocturnal, not even his 
family may know of his trouble. Whether they occur during the day 
or night, it sometimes happens that the patient has no very distinct 
knowledge of them, particularly when they begin or are first discovered 
by the friends. In some forms of the disease in which the psychosis 
is the predominant element, the patient's own diary written by him 
while in the epileptoid state is a surprise to him. In petit mal he is 
usually unaware of his attack and when it is over goes on about his 
business as though nothing whatever had taken place. Very often 
early in the onset of even the seizure types of the disease the patient 
has only a vague sort of idea that something has happened. I have 
actually been asked thus by epileptics, especially those who have had 
their attacks at night, what could have happened to have caused their 
tongue to be so sore and jagged. It is almost pathetic at times to 
observe, especially in the young, this wonder, mystery and confusion, 
nay, even total ignorance and indifference sometimes, displayed by 
those who are apparently unaware of the nature of their trouble. In 
such cases the testimony of friends and witnesses of the attacks alone 
has to be depended upon for an account of the disease. The signs are 
all objective, the subjective being so slight or swallowed up in the 
period of overwhelming unconsciousness that the patient himself can 
give no intelligent account of himself. If the attack is thus capable 
of being verified and is typical, epilepsy can be positively diagnosed. 
That does not mean, however, that the attacks alone constitute the 
disease and the patient may not be the victim of it without the actual 
occurrence of the typical fits. 

There are cases that are undoubtedly epileptic, as are shown by 
the later appearance of the typical fits which in the meantime have 
gone on exhibiting for years periodical attacks of severe headache, 
asthma, cardiac disturbances, local and visceral neuralgia, unaccounta- 



THE NEURONIC DISEASES 1 97 

ble moods and spells of eccentricity, vomiting, nocturnal pollution, 
nightmare and other so-called epileptic equivalents. In such cases 
these manifestations may awaken the suspicions of the medical at- 
tendant, but cannot in any way constitute the basis for a* diagnosis of 
the disease. Only the typical fit can afford such a basis. 

How often have we all sought in vain for an earlier evidence of 
the disease in which the first typical outbreak occurred well along in 
adult life, knowing all the time that it was a hereditary trouble and 
should have given some warnings in the earlier years of the patient's 
life ! And how often have we been almost inclined to doubt the pos- 
sibility of finding any pronounced underlying neuropathic premonition 
in the history of the patient's life until we were volunteered the state- 
ment that an abnormal periodical hunger and freakishness of appetite, 
a dysmenorrhcea without any apparent organic cause for it, an oc- 
casional insane outburst of ungovernable temper, or a peculiar, irresisti- 
ble impulse to do and say certain things, have been noted ! 

Epilepsy is a much-abused term and many and varied are the 
phenomena that have been recorded under it. Many diagnosticians 
have come to deny the wisdom even of ever declaring the presence of 
the disease until more than one fit has actually been observed by him 
who is called upon to make the diagnosis. This seems to be rather a 
tightly drawn position to take, and yet it was inevitable almost from 
the loose manner in which every form of convulsion and mental oblit- 
eration was looked upon as epileptic. My own position is that epilepsy 
is present in the patient as a distinct, positive disease even when there 
are no fits as yet in evidence ; that in such cases the equivalents of 
the disease may awaken suspicion and put the physician on his guard; 
but that only upon the occurrence, all other things being considered, 
of the actual typical attack, varied even as this may be, should a posi- 
tive diagnosis ever be founded. If possible the physician himself 
should see the attack, and better still, more than one ; nevertheless if 
those describing it to him are honest, observant and intelligent indi- 
viduals, he may base a positive diagnosis of the disease if their account 
presents a clean-cut, typical picture. Too much caution, however, 
cannot be exercised by him in making his diagnosis in such a way, 
for epilepsy is a disease often simulated by malingerers and so closely 
resembles other diseases, or is so closely imitated by other diseases, 
that even the most intelligent of the laity will give a description with 
all honesty of it such as to mislead the medical man into pronouncing it 
genuine epilepsy. 

In nearly all cases there are premonitions of an attack. These 
may be very pronounced and exist for several minutes, hours or days. 
On the other hand, they may be so slight and brief that they are not 
recognized by the patient or spoken of until after a most searching 
inquiry is made by the examiner. In some cases no premonitory signs 
can seem to be discovered, though I have found that these cases have 
gradually diminished in number as I have learned to make my exam- 
inations more searching. 

These forewarnings may be studied under the heads of sensory, 
psychic, motor and irregular aur?e. 



I98 THE NEURONIC DISEASES 

The term aura is particularly applicable to the sensory premoni- 
tion, for there is a suggestion of a sort of ascending "spirituous vapor" 
which Pelops, the master of Galen and first user of the name, sup- 
posed passed up through the extremities to the head by way of the 
veins. A peculiar sensation starting in the toes or tips of the fingers, 
from the stomach or region of the heart, and rapidly and lightly sweep- 
ing up towards the head, is very often felt just before the stroke of 
unconsciousness falls. The sensation is varied and uncertain. Many 
patients declare it is indescribable, especially the very frequent gastric 
form of it. It may resemble the globus of hysteria or retching. At 
other times it may consist of actual pain, especially in the vicinity 
of the heart. In the limbs it consists of some form of paresthesia, 
such as tingling, pins-and-needles sensation, formication or numbness. 
There may be slight dull headache. Not always does this sensation 
ascend ; occasionally it descends. It may not appear at all or in aborted 
attacks it may die out without the onset of any other symptom what- 
ever. 

When it was thought at one time that this sensory aura was 
somehow the direct cause of the fit, bands were tightly drawn around 
the arm and leg to check its progress. As in a certain percentage of 
cases this manoeuvre was followed by an aborted attack, the belief 
in the causative influence of the aura was strengthened as the result of 
a sort of post hoc propter hoc reasoning. 

It is usually stated that these sensory forerunners of the attack 
occur in about half of all the cases. I am skeptical of all statistics 
founded upon subjective phenomena, and especially upon such varied, 
elusive and intensely personal phenomena as are the sensory aurae of 
epilepsy. I have a suspicion they are present in more than half the 
cases, for I have not infrequently learned of them in long-subsequent 
visits upon the patient or from the testimony of friends with better 
memories, or in other direct and indirect ways when the closest ques- 
tioning of the patient himself, who may have belittled or forgotten 
them, failed to elicit their existence. 

After the general sensory aurae the most frequent and important 
are those of the special senses. Of these vision furnishes the largest 
number. Flashes of light, fortification figures, stars, lightning-like 
lines, increase and diminution in the size of objects, bright colors and 
darkness are all mentioned. Actual hallucinations and real pictures, 
curious illusions, the vanishing and approaching of persons and things 
are epileptic aurae that go a long way to explain some of the wonderful 
assertions of mystics, religious devotees, hysterical recluses and other 
superstitious neuropaths. Much fascinating and romantic literature, 
especially in the Middle Ages, when religiosity was rampant and 
ignorance was its handmaid, has been written on the basis of these 
visions. 

In the sphere of smell and taste some extraordinary phenomena 
are sometimes met with, though usually the patients who experience 
them describe them as bitter, sweet, pleasant, disagreeable, metallic, etc. 
Numbness of the tongue and palate may occur. One of Spratling's 
patients spoke of the aura as "a snuff of bad air." 



THE NEURONIC DISEASES I99 

Xext to the visual the auditory aurae have furnished the strangest 
and most weird descriptions. Xot only noises, but the ringing of bells, 
blowing of whistles, sweet music, voices, human speech and other 
sounds, both in and out of nature, pleasant and terrifying, are heard. 
It is easy to conceive how these may be the basis of heavenly com- 
mands, spiritualistic whisperings and divine inspirations. The range 
of the auditory aurae stretches all the way from intolerable roaring and 
shrieks to actual deafness. 

Were these special sense aune only more frequent than they are, 
and did they occur relatively more often in the grand mal type of the 
disease, they would probably be less mysterious and therefore less 
misleading to the ignorant and superstitious laity. The visual aurae 
are twice as frequent as all the other special sense aurae combined ; 
the auditory are one-quarter as frequent as the visual ; the olfactory 
and gustatory are the least frequent of all. Usually only one sense is 
affected; rarely, however, two or more senses may exhibit aurae simul- 
taneously. 

Still more astounding at times than the sensory aurae, though 
they are less frequent, are the psychic. The mental processes, especially 
the imagination and intellection, are unusually quickened. Emotions 
of a high degree, and a rapid succession of ideas, spring into being and 
continue until suddenly obliterated by the paroxysmal stroke. It is to 
be remembered that the sudden, unaccountable actions of the patient 
may be due to the nature of these exalted feelings and ideas. Fear and 
horror may cause him to suddenly run away or strike at a neighbor, 
or accomplish his own destruction. It must be undoubtedly true some- 
times what we are told of the sudden illumination and inspiration which 
these patients experience when they are composing, inventing or 
attempting the solution of some abstruse problem. The fine frenzy of 
the poet may sometimes be closely allied to a psychic aura. Memory 
may be exalted, so much so that the far past is regarded by the patient 
as being actually the present. 

These aurae are at times delirious and seem like a veritable pre- 
epileptic insanity. The}- are mostly of the depressive and terrifying 
type, though they may be of the exalted and ecstatic type with rapture, 
joy, lightness or immense serenity. Spratling quotes from Dostoievsky, 
the Russian novelist, who was himself an epileptic and described his 
own feelings in the character he has drawn in "Besi". "There arc 
moments, and it is only a matter of five or six seconds, when you sud- 
denly feel the presence of eternal harmony. This phenomenon is neither 
terrestrial nor celestial, but is an indescribable something which man 
in his mortal body can scarcely endure. The terrible thing is the 
frightful clearness with which it manifests itself and the rapture with 
which it fills you. During those few seconds I live a whole human 
existence." 

It is but a step from this to the belief in and proclamation of one's 
power of disembodiment and visitation to the supernatural. 

Psychic aurae, like the sensor}-, are to be awarded the credit of 
giving us many strange beliefs, surprising mental exhibitions and what 



200 THE NEURONIC DISEASES 

seems almost like omnipotent clairvoyance. It is just here where 
genius unto madness becomes closely allied. 

The motor aurce consist of jer kings, local spasms, trembling, 
twitching in one or more limbs. They are very brief as a rule and are 
more characteristic of partial or Jacksonian epilepsy. Complicated 
coordinated movements of an automatic sort are occasionally observed. 

Procursive epilepsy is that form in which the patient runs forward 
just before the fit. Some epileptics turn rapidly around and go around 
in a circle. Gould and Pyle relate the case of an epileptic workman 
who, upon one occasion, ran from Peterboro to Whittlessy. A patient 
of Echeverria's resorted quickly to violent exercise on a trapeze to 
control the spasms. A patient of mine would jump up and run around 
the dinner table. 

There are many other premonitory signs of the disease classified 
under the head of irregular aura. A sudden pallor, general erythema 
or spotted appearance of the skin may represent a vasomotor aura. 
Profuse perspiration has introduced a fit. A case reported by Moyer 
was wont to have sudden attacks of uncontrollable sleepiness. This 
somnolence has been noticed in a number of cases. 

Elevation of general and local temperature, and sphygmographic 
evidence of increased arterial tension have been observed during an 
aura. 

Immediately succeeding the aura or, as in some cases, without it, 
the patient abruptly falls in a state of complete unconsciousness. He 
may fall in any direction, though usually it is forward. He may strike 
any near object, such as a hot stove or sharp point and thus acquire a 
wound that may leave an ugly scar. A young woman patient of mine 
was found dead, having dropped while making the bed in such a way 
that her throat and chin became caught on the sideboard of the bed- 
frame and she was asphyxiated. 

With the fall and the sudden coma there is a tonic spasm or sudden 
tetanic stiffening of all the muscles of the body. The teeth are 
clenched, the arms are rigid and flexed, the thumb is pressed tightly 
down into the palm of the hand and the fingers firrnly flexed on top of 
it, the legs are stiff and flexed or extended. The limbs are not all 
contracted in the same way. The patient appears therefore contorted 
and hideously deformed. The trunk is twisted or arched. The head 
is turned to one side, the facial muscles drawn or distorted, the eyes 
fixed with the lids closed or open and the pupils immoble, or the eye- 
balls rolled up into the head, the lips compressed and distended laterally, 
the cheeks bloated and disfigured and the color pale and cyanotic. 
Frothy saliva, mixed with blood if the tongue happens to have been 
caught between the snapping teeth, sometimes oozes between the par- 
tially opened lips. The muscles of the neck are rigid and marked in 
outline. On account of the spasm of the laryngeal and respiratory 
muscles a short, sharp, piercing cry, or perhaps only a loud sigh, is 
heard. The breathing ceases or becomes a mere inspiratory gurgle. 
The faeces and urine may be involuntarily extruded. 

After a few seconds or fraction of a minute this first or tonic stage 
is followed by the second or clonic period. The unconsciousness con- 



THE NEURONIC DISEASES 



201 



tinues or may even clear up a little, or may have been only partial from 
the beginning. The face becomes flushed. The muscles of the entire 
body twitch and jerk forcibly and rapidly in a rhythmical sort of a 
way. On account of this the patient may be thrown violently about, 
some of his joints be dislocated or even a bone be broken. These 
movements are at times very powerful, symmetrical and regular. The 
jaw snaps and the tongue, being pushed forward, causes the teeth to 
lacerate its edges. The eyeballs roll about. The rectum, bladder and 
seminal vesicles may all be evacuated. The respiratory movements 

FIGURE 38. 







m\ 






WBE^jH 




P"^^^^^E. 


g 


W^fr 




*m» 




fcii 




>^r 


r^P 




^^^^ 


f 



Grand mal seizure, with partial retention of consciousness. (After Spratling.) 



become heavy and sighing. Vomiting and retching may occur. The 
pulse increases in frequency along with the respirations. Perspiration 
breaks out over the whole body, and the general appearance of the 
patient shows a beginning relaxation. The vise-like hold upon him in 
the tonic stage is clearly letting go dining the clonic stage. 

Towards the end of the clonic stage, which lasts from one to five 
minutes, the muscular movements gradualh quiet down, cease entirely 
in some muscles and in all of them later on, and the patient lies limp 
and exhausted. Sometimes he opens his eves, looks dazed and eon- 
fused, and then sinks into a profound slumber; at other times lie seems 
to suddenly regain complete consciousness, bul is surprised and com- 
plains of an intense headache and of feeling very tired and sleepy. 
•Somnolence may last several hours and constitutes what is some- 



202 



THE NEURONIC DISEASES 



times called the third stage of the attack. The sleep is so natural and 
physiological after such a profound expenditure of nerve force, while 
the rest of the patient's condition is so little disturbed, that the pro- 
priety of calling this the third stage of the paroxysm may well be 

FIGURE 39. 




The order of progression of attack in a case in which the initial spasm — 519 
times in succession in forty-nine hours — was confined to the first phalanx of the 
right thumb. (After Spratling.) 

questioned. From this sleep the patient usually wakes up refreshed, 
with his normal consciousness completely restored and only a slight, 
decreasing headache and possible soreness of the tongue indicating to 
him that something unusual has happened. 



THE NEURONIC DISEASES 20} 

Such is the general sequence of events in a typical grand mal 
attack. There are variations upon this clinical picture that must now 
be noted. 

In the tonic stage of the fit the tetanic rigidity of the muscles may 
be so powerful, and the cessation of the respiration so prolonged, that 
•death will occur under the most extraordinary circumstances. A 
woman once w r ashing dishes at a sink made a noise that attracted 
attention, and when discovered a little while after was found dead 
rigidly standing in the same position. Relaxation occurred after they 
laid her on the floor. 

Sometimes in this stage a fine series of fibrillary contractions can 
be detected in the muscles. All muscles of the body may not be equally 
stifT and in exceptional cases only those of one side have been involved. 
It is not so very uncommon, even in the so-called idiopathic types of 
the disease, for the spasm to begin in one limb or on one side of the 
body. This peculiarity, with others, wdiich indicates a close resemblance 
between idiopathic and symptomatic epilepsy, gives ground for the 
contention of Starr that epilepsy is an organic disease and that there 
is no such distinction as the above between types. The ciliary muscles 
of the eye are also sometimes included in the spasm (Knies). 

When they can be tested the reflexes are found to be abolished 
during the tonic stage. They have been seen to be normal and even 
exaggerated but in these cases the unconsciousness and general sup- 
pression may not have been profound. The conjunctiva is insensitive 
and the pupils are dilated and irresponsive. The fundus oculi has been 
observed to be pale, then flushed. Thomsen and Oppenheim have 
shown that not rarely concentric contraction of the visual field follows 
true epileptic attacks. Transient paralysis, aphasia and dysarthria may 
immediately succeed a fit. 

The skin and mucous membrane may be red in spots and exhibit 
minute hemorrhagic extravasations. After the attack the urine may 
be discharged in excessive amount, may contain an increase of urea 
and some albumin. A slight elevation of temperature may be noted 
during the fit. High temperature belongs to the symptomatology of 
status epilepticus. Cases in which there are marked and persistent 
post-epileptic phenomena, such as aphasia, paralysis, tremor, conjugate 
deviation of the eyes, blindness, deafness, diarrhcea and vomiting, 
should always be regarded with a high degree of suspicion. True 
epilepsy may not be the cause of them but rather some gross lesion 
such as tumor, thrombosis or hemorrhage. 

After these grand mal attacks have once started they tend to re- 
appear periodically, and increase in number and severity. For a time 
they are nocturnal, occurring mostly in the early hours of the morning 
while the patient is sleeping and the physical forces are at their lowest 
ebb. Sometimes they take place just after retiring at night. As the 
disease continues they appear in the daytime and often cease ;it night. 
Usually they are single but two or three attacks in succession ma\ 
cur the same day or on successive days. These serial attacks may be 
so numerous, rapid and close together that a condition of >t-un- 
■set up. Some patients have grand mal attacks every few weeks or 



204 



THE NEURONIC DISEASES 



months, with many fits of the petit mal type in the intervals. Rarely 
a patient may experience a fit only once or twice in a year or two. 

A most interesting and singular form of epilepsy is that which 
appears in the petit mal type. This is characterized by frequent, brief 
disturbances of the consciousness, entirely unknown to the patient and 
without aurae and convulsions. The attacks come on without the 
slightest warning and may occur several times during the day. The 
patient suddenly stops his work, becomes fixed and staring and seems 
to be in a profound condition of mental abstraction. This lasts but a 
few seconds and when it is past the victim proceeds with his occupa- 
tion just as if nothing whatever had happened. Bystanders, however, 
can note the fixity of the attitude, the partial or complete absence of the 
consciousness, the momentary cyanosis, the strange appearance of the 
patient and even the slight momentary spasm. In rare cases there may 
be a feeble aura of some sort, or the spasm may appear transiently 
without loss of consciousness. In other cases the mind is not so much 
absent as diverted. The patient responds but his answers are irrele- 
vant. He may stop in the middle of a sentence and mumble words 
about something entirely different, or he may automatically get up 
from his desk and do something else. If he is directing envelopes, for 
instance, he may suddenly awaken to discover that he has directed an 
unnecessary number all exactly alike. In such attacks there is usually 
partial amnesia, the patient dimly remembering that he was doing 
something different, but what or why he cannot understand. There is 
an automatic, dream-like state under such circumstances in which the 
sufferer may do all sorts of queer things, such as undressing himself 
in public, striking those about him, walking off of dangerous heights 
and writing long compositions. 

These states may be prolonged for several days, weeks or months,, 
enabling the patient to travel long journeys, transact elaborate busi- 
ness and do 1 a lot of strange things, of all of which he has only the 
vaguest sort o>f remembrance when he suddenly comes to and finds him- 
self in the midst of strange surrounding sand anomalous positions. The 
cases of so-called double consciousness such as that of Alary Reynolds,, 
reported by Weir Mitchell, and of lima S., studied by Krafft-Ebing, 
are of this character. 

The general mental state of these patients, except when they are 
in the fit, is not as a rule much below the normal. In fact the posses- 
sors of the most brilliant minds have sometimes been the victims of 
both grand mal and petit mal attacks. Caesar, Mahomet and Napo- 
leon are the classical illustrations. As a rule, however, there is apt to 
be more mental deterioration among the petit mal than among the 
grand mal epileptics. In the former there may be terrific outbursts 
of passion and violence, with the commission of great crimes. A 
veritable delirium and mania may even occur, or there may be a pro- 
found dementia. Instead of violence a low cunning treachery may be 
exercised in the attainment of their strange purposes. 

There is an obvious medico-legal interest surrounding these cases> 
The degree of consciousness or its perversion should, of course, deter- 
mine such a patient's criminal responsibility. This problem being so 



THE NEURONIC DISEASES 205 

-difficult, one need not feel surprise at the unfortunate wrangles that 
sometimes mar the court proceedings when so-called expert testimony 
is being taken. 

Some of these attacks are less of the type known as petit mal 
than they are instances of what are known as the psychic equivalents 
-of epilepsy. 

The whole question of epileptic equivalents is still under discus- 
sion. By the term is meant something that is not so much like an 
epileptic fit as that it is a substitute for it, equivalent in value, force, 
meaning, compensation, etc. Most writers recognize the existence of 
■epileptic equivalents, though Magnan, Le Grand du Saulle, Tomlin- 
son and others deny them. The psychic equivalents do certainly at 
times seem more like states of insanity, perhaps post-epileptic insan- 
ity. The propriety of characterizing these states as epileptic is doubt- 
ed for the reason that when they are not associated with typical fits 
they are rarely if ever so characterized but are then looked upon as 
■distinct psychoses or pure mental disorders. However, as epilepsy is 
in some respects so largely a mental manifestation, it is not easy to 
deny that a psychosis ma}' be truly of epileptic origin. Hence for the 
present, at least, it will be well to speak of the epileptic equivalents, 
-especially those in the psychic sphere. 

Spratling desires to keep a sharp distinction between true psychic 
epilepsy and the psychic epileptic equivalents. The distinction rests 
upon the presence or absence of other epileptic signs such as the motor 
•disorders. 

Among the equivalents, the psychic always far outnumbering all 
the others, may be mentioned the absences, the strange acts, the in- 
decent exposures, the mild manias, such as nymphomania, klepto- 
mania, etc., certain phobias and obsessions involving unprovoked as- 
saults, automatic laughter, a form of angina pectoris, diaphragmatic 
spasm, sleep states, asthmatic affections, spasm of the glottis, nocturnal 
pollution, certain forms of pertussis, neuralgias, migraines, the hunger 
-evil, sudden outbreaks of perspiration, verbigeration, etc. 

There is such a thing as reflex epilepsy but not in the sense of 
the old writers. A dormant epileptic condition may be aroused into 
activity by various exciting peripheral irritants, but a true epilepsy 
can hardly be attributed to the mere excitation produced by such peri- 
pheral disturbances. In a person predisposed it is conceivable that 
a phimosis, a cervical uterine scar, a mass of intestinal parasites, a 
nasal polyp, a pharyngeal adenoma, an accumulation of wax in the 
«ar, and muscular anomalies of the eye, may be the cause of initiating 
the attacks. To say that such conditions can be the cause of epilepsy 
in non-predisposed individuals would have to be followed by an 
planation, before the assertion could be accepted, as to why more suf- 
ferers from these common conditions do not have epilepsy, and why 
in those that do have epilepsy from this condition there are always 
found the great predisposing factors of heredity, degeneracy, intoxi- 
cation or trauma. 

Oppenheim notes that binding a limb <>n which there is a peri- 
pheral cicatrix will often check an epileptic fit. Hie same thing will 



206 THE NEURONIC DISEASES 

often occur, however, in so-called simple idiopathic epilepsy without 
any such peripheral irritant. The scar in such a case may indeed be 
a sort of epileptogenous zone, but that does not establish it as the 
sole or prime cause of the disease. 

I find there is not a little confusion in the minds of some of the 
profession between partial, or Jacksonian epilepsy, and what is called 
symptomatic epilepsy. 

Every form of local convulsion is not partial epilepsy. It may not 
be epilepsy at all but merely epileptiform. In a way it may be physio- 
logical rather than pathological, for it may represent the normal over- 
action of a vigorous and healthy sensory-motor apparatus to an ex- 
ternal source of constant irritation. So-called symptomatic epilepsy 
is therefore but a convulsive symptom of the disease of which it is 
declared to be symptomatic. A compressing lesion of the foot, say, 
causing pains and spasms in the area of the nerves caught in the lesion 
does not necessarily cause those pains and spasms to be symptoms of 
a nervous disease. This is an important distinction to bear in mind 
when speaking of partial, or Jacksonian, epilepsy. This, unlike mere 
symptomatic epileptiform manifestations, is a true nervous or cere- 
bral disease and is epilepsy. It may originate remotely from the irri- 
tation, disturbed circulation or other influence from an extra-neural 
growth or lesion of some sort. Gradually, however, a local change is 
set up by this extra-neural influence so that the pathological basis of 
a true epilepsy is established. This change may remain local, more 
often it spreads throughout the entire cortex. 

The great characteristic of Jacksonian epilepsy, therefore, is its 
local distribution, either during the entire fit or at its commencement. 
The sensory or motor phenomena begin in one arm or leg, one fin- 
ger or side of the face, then increase with or without the loss of con- 
sciousness through the entire epileptic cycle. This is not a mere aura, 
though it may partake of the nature of one if the fit passes into a 
general one involving the mind and body, as in the ordinary grand mal 
type. It is, in the purely local cases, the epilepsy itself. Hence we 
see the propriety of the term partial epilepsy. 

As I have said it may remain partial and be free of any asso- 
ciated disturbance of the mind. In most cases, however, the loss of 
consciousness comes on, somewhat more slowly than in the grand mal 
seizures of the idiopathic type, and then the patient experiences the 
typical generalized convulsive seizure. The pre-eminent fact in re- 
gard to it is that the localization of the phenomenon never changes. 

These cases are usually followed by more or less persistent local 
physical defects such as paresis, paresthesias, aphasia, etc. 

Their causes are numerous and may be purely local or general. 
Among those that have been enumerated I may instance injuries to 
the skull involving the brain, cerebral hemorrhage with its pathological 
sequela?, thrombus, embolus, syphilitic meningitis, tumor, alcoholic ox- 
cess, old cicatrices and visceral sources of irritation. This does not 
exhaust the list but indicates a few ways in which, the cortical cells 
may be rendered epileptogenetic. 

There has always been a discussion among writers as to whether 



THE NEURONIC DISEASES 20J 

simple tonic or clonic convulsions alone can constitute epilepsy. Prich- 
ard described, in 1822, a violent and powerful form of epileptic 
seizure in which a tetanic state of the muscles occurred. These cases 
are rare, fortunately so, for they are very fatal. It seems to me that 
Prichard described simply an exceptionally severe type of grand mal 
in which death occurred during the prolongation of the tonic stage, 
and before the appearance of the clonic stage. 

The myoclonus-cpilcpsy, described by Unverricht in 1891, is an 
association disease or trouble like hystero-epilepsy, choreic epilepsy, 
etc. The two diseases may run together in the same patient, with 
alternation or combination of the symptoms. The association, how- 
ever, does not constitute a new disease or special type of either. Occa- 
sionally the disease is really one thing with a mere resemblance in 
some of its phenomena to the other. Hystero-epilepsy, for instance, 
is usually hysteria whose outbreaks resemble at times epileptic seiz- 
ures. It serves no useful purpose, and is only confusing, to establish 
new diseases or even new types of mere associated or similarly appear- 
ing affections. 

Much stronger is the ground, if types are to be noted, for sepa- 
rating status ipilepticus as a special form of the disease. Clark de- 
fines it as the maximum development of epilepsy in which one 
paroxysm follows another so closely that the coma and exhaustion are 
continuous between seizures. Sooner or later there is a marked eleva- 
tion of temperature, pulse and respiratory movements, with profound 
exhaustion and death. 

Status occurs most frequently in the grand mal type of the disease 
and partakes of all the features of the disease except in regard to the 
special points above noted. 

To treat it as a separate disease with its own etiology, pathology, 
symptoms and treatment is quite unnecessary. It is a culmination of 
epilepsy and is distinguished by differences of degree rather than kind. 
The patient remains continuously unconscious. The muscles appear 
to be almost continuously convulsed. The temperature may rise to 109 
degrees F. and even recovery occur, as in a case reported by Spratling 
at the Craig Colony. 

About half the cases that attain the condition of status die. 

Among the sequela of epileptic convulsions are to be noted the 
scars upon the tongue and about the face and body, extensive burns, 
fractures, dislocations, hemorrhagic extravasations, exhaustion, paraly- 
ses, elevation of body temperature and certain changes in the blood 
and the circulation. Some of these, especially the apparent increase 
of toxicity in the blood and elevation of the blood pressure, need fur- 
ther investigation. 

The mental sequelec of single and multiple epileptic seizures is 
always a matter of great anxiety to the patient and his family. It 
would not seem reasonable to expect so profound a disturbance of the 
cerebral functions to continue long without some deterioration of the 
mental faculties. Depression, mistrust, irritability, melancholia, and 
increased emotionalism are usually noticeable in these patients. The 
mental condition may get no worse than this, and may indeed even 



208 



THE NEURONIC DISEASES 



seem to be not in the least affected for years. Later on the memory 
grows weaker, amnesia occurs, the intelligence becomes blunted, more 
or less stupidity supervenes and ultimately simple dementia appears. 
Hypochondriasis is often present. The mental deterioration charac- 
teristic of the disease I am convinced has been too often charged to 
the use of bromine. 

When the disease occurs in childhood the mental results are for 
obvious reasons much more disastrous. Imbecility and idiocy are espe- 
cially liable to occur. All forms of the disease without distinction are 
responsible for the lowering of the intelligence. Some have thought 
that there was more danger in this respect in the petit mal than in the 
grand mal, but it is to be remembered that the petit mal type of the 
trouble is almost always entirely psychical. It represents as it were 
a considerable degree of mental degeneracy in itself. 

As bearing on the treatment it is to be noted that sometimes epi- 
leptic seizures are followed by a disappearance of a certain amount 
of stupor and mental indifference. I have long taught in my lectures 
that it is not always wise or safe to suppress completely and perma- 
nently the fits even when that is possible. Occasionally an epileptic 
who shows himself amenable and responsive to treatment is better off 
for a fit now and then. 

Diagnosis. Epilepsy is usually easily diagnosed. In doubtful 
cases it should never be hastily decided. The longer a case is ob- 
served the more the diagnosis becomes conclusive. It is when the dis- 
ease is first discovered, and when it is wanting in some typical mani- 
festation, that the diagnosis sometimes becomes problematic. For this 
reason and because of the serious prognosis attending the disease, the 
physician will do well to rarely make a positive diagnosis until he has 
been able to watch the patient in one of his attacks. The laity are so 
easily misled, being untrained and excitable, that it is never wise, ex- 
cept possibly in certain very obvious instances, to risk a diagnosis upon 
the description of friends or relatives. The earlier it is in the disease 
and the more atypical the account of it seems to be, the more impera- 
tive is it that the diagnostician should see the fits for himself, or 
should place the patient where he can be under the continual observa- 
tion for a time of a trained assistant. Under such circumstances every 
detail, however insignificant it may seem to be, should be made 
note of. 

The presence and character of the aura? should receive the most 
scrutinizing attention, for the very nature of the disease and its source 
may be indicated in the aura. Then the mode of onset should be care- 
fully observed. This will include the relative period at which the 
unconsciousness took place, its depth and duration ; the location of 
the first convulsive manifestation, its extension over the rest of the 
body, its tonic and clonic character, its duration and its mode of dis- 
appearance ; the state of the pupils ; the condition of the eyes ; the 
strength and frequency of the respirations and pulse beat; the cyanosis. 
followed by flushing of the skin ; the involuntary evacuations of the 
bowels and bladder. 

The character of the after effects will in some cases help to estab- 



THE NEURONIC DISEASES 2(X) 

lish the diagnosis. They are the return to a dazed and surprised state 
of consciousness, the headache, the profound exhaustion, the transient 
paralyses, local muscular soreness and even slight mental aberration. 

In every suspected case of epilepsy, whatever the type, look for 
some disturbance of the consciousness. This is undoubtedly the car- 
dinal symptom of genuine epilepsy. It may be the sole symptom, as in 
some cases of petit mal, psychic epilepsy and the psychic equivalents 
of the disease. It is even detectable in the cases of partial or Jackso- 
nian epilepsy in which the motor manifestations ma}- be almost over- 
whelmingly dominant. 

Xote the character of the disturbance in every particular and the 
order of its progression for it is pathognomonic of the disease and 
is never exactly the same as it is in other diseases. If it is accompanied 
by the convulsions and other usual symptoms of a lit. the diagnosis 
is absolutely easy and certain. 

A good deal is written about the fades epHeptica. Many epileptics 
show in their faces the indications of a degenerative heredity, as I have 
often pointed out to my classes. They also exhibit scars acquired by 
falls and injuries sustained in previous attacks. They may even re- 
veal the facial acne from the overuse of the bromides. All of this, 
however, is of no very great value in the matter of diagnosis for with 
such conditions present the case is apt to be a pronounced and ad- 
vanced one, and doubtless already easilv diagnosed from the other 
symptoms. As the Upical facies epileptica is not an early, sudden 
acquisition, but rather the result of a slow development, it cannot as- 
sist us much at that period in the disease when such assistance is most 
needed, and when the diagnosis of the disease is of the supremest im- 
portance. 

There are a number of conditions in which mental and motor 
disturbances occur, with which an epileptic attack is capable of being 
confused. They are hysteria, alcoholism, drug intoxication, syncope, 
uremic poisoning, cerebral apoplexy, general paresis, vertigo, tetanus 
and simulation. 

The differentiation between hysteria and epilepsy is at times a 
matter of great importance and difficulty. There are convulsive seiz- 
ures sometimes in hysteria so like those of epilepsy that, for a long 
time the}' were studied apart under the name of hystero-epilepsy. The 
one manifestation that can be absolutely relied upon to establish the 
distinction is the pupillary reaction. In hysteria this is not lost as it 
invariably is in epilepsy. Hysteria being a psychosis primarily the 
whole complexion of the case is dominated by the mentality of the pa- 
tient ; in epilepsy the mental disturbance is the result of a frank cerebral 
lesion and is therefore often accompanied by marked localization phe- 
nomena. In other words the mental side of the picture and a certain 
suggestiveness of active volition are more noticeable in hysteria, 
whereas in epilepsy the convulsions or motor phenomena and appear- 
ance of complete absence of volition stand prominently forth. The 
suddenness of the attack, the initial cry. the involuntary twitchii 
the injury from the fall, the mvoluntarv evacuations, the subsequent 
exhaustion, stupor, headache and somnolence all point t<> epilepsy. 



210 



THE NEURONIC DISEASES 



Hysterics do not injure themselves by falling unconscious nor do they 
often bite their tongues. Involuntary micturition practically never oc- 
curs in hysteria. Hysterics yell and cry and toss themselves about and 
complain of pains and develop their attacks at the time of day, early 
evening, when they are likely to be observed. Their attacks are longer 
in duration than those of epileptics and are sometimes amenable to 
sharp suggestion. Their symptoms vary during the attack and have 
prominently among them sensory phenomena. 

The mental criteria are of some value as hysterics are usually 
keen and intelligent, whereas epileptics, especially of long standing, 
are dull, somnolent and even demented. The facies epileptica is not 
exhibited by hysterics nor do they ever have the post-epileptic paraly- 
sis, hemorrhagic extravasations, wounds, mental confusion and auto- 
matism that epileptics often show. They never develop a temperature 
of a degree or two, such as occurs in the epileptic. On the other hand 
they recover promptly, pass large quantities of urine after the attack 
and assume an entirely different manner when the causes of the initia- 
tive a emotion out of which the attack grew are removed. A motive 
lurks behind many outbreaks of hysteria, and as the attack is thus 
somewhat in the sphere of volition, painful pressure upon the ovaries, 
threats of discomfort and objectionable manoeuvres will often bring 
a hysterical convulsion to an abrupt termination. 

The coma of acute alcoholism is not so complete as it is in epilepsy 
and there are no typical convulsive movements. The odor of the 
breath, the flushed face, the maudlin semidelirious state, and the ab- 
sence of most of the characteristic symptoms of epilepsy, such as the 
pallor, the turned-up eyes, the bloody frothing at the mouth, the rigid 
condition of the muscles, etc., all distinguish the one disease easily 
from the other. 

Urcemic, drug and lead intoxication are to be distinguished by 
the usual history of disease in other organs, of drug-taking and occu- 
pation in lead. 

Syncope occurs in feeble individuals and under special surround- 
ing conditions such as an over-heated room, shock, over-exertion. 
Heart disease is often present. Syncope is wanting in the usual signs 
of epilepsy, such as the aura, the muscular spasm, the initial moan, 
the evacuations and the usual sequelae of stupor, headache and somno- 
lence. The faintings come and go, several in succession, like a soft 
zephyr without causing much disturbance in the patient's attitude. 

The paralytic symptoms, the history of the onset, the action of the 
pupils, the respiration, the duration of the coma, with the absence of 
many of the symptoms of epilepsy, will help to distinguish the cerebral 
apoplexia from the latter. 

Aural vertigo, or Meniere's disease, is accompanied by aural symp- 
toms such as tinnitus and deafness. 

In the early stages of dementia paralytica the convulsions are apt 
to be unilateral, and not accompanied by a loss of consciousness. There 
are other well-known symptoms, such as the tremor, the emotionalism, 
the eye symptoms, that enable us to recognize general paresis. 

However, it is to be remembered that in general paresis, tumor, 



THE NEURONIC DISEASES 21 1 

cerebral syphilis, nephritis and arteriosclerosis the epileptiform con- 
vulsions are more apoplectic and symptomatic than are the evidences of 
genuine epilepsy. Therefore, always search well for the symptoms of 
these diseases and regard the convulsions as wholly one of these symp- 
toms. In other words, the examination is not so much to determine the 
differential diagnosis between an idiopathic and symptomatic epilepsy, 
so-called, as it is to determine the diagnosis of the disease of which 
the epileptiform manifestation constitutes one, and perhaps a minor, 
evidence. 

In tetanus there is generally a history of an injury, and the jaws 
are characteristically locked. 

Simulation sometimes causes quite a little trouble. To escape 
punishment for a crime, or to win large damages from a railroad or 
other corporation, are two powerful motives to tempt cunning persons 
to study and imitate epilepsy. Usually their detection is easy, but I 
have seen the fraud so skillfully practiced that the shrewdest exam- 
iners were deceived. 

If closely watched a simulator will omit or perform wrongly some 
one manifestation among the many that he has to remember. For 
instance he will not close his thumb down and clench it beneath his 
fingers, or he will forget the cry, or fail to bite his tongue. His re- 
flexes will be lively, especially his pupillary reactions. He will ex- 
hibit no scars, no hemorrhagic extravasations, no petechial spots. 
There will be no involuntary evacuations, nor will he suffer afterwards 
with an exhaustion paralysis, a stupor and prolonged somnolence. His 
body temperature will not rise. He will tend to overdo the part and 
elaborate symptoms that should be kept in abeyance, or make little 
of those that should be very prominent. Without seeing the patient, 
so-called, I detected a very cunning simulator once in a long hypothet- 
ical question constructed to correspond with the case, because one part 
of the clinical picture did not harmonize with another part, whereas if 
each had been presented alone without the other the deception would 
have been much harder to detect. 

Mai ret emphasizes the importance of a urinary analysis. The 
toxicity of the urine is said to be decreased after the attack, and ren- 
dered hypotoxic in the intervals of true epilepsy. 

Spratling points out that a simulator can reproduce the tonic bet- 
ter than he can the clonic contraction. 

Heller has suggested that the thigh, for instance, be firmly grasp- 
ed, and in a simulator the muscles will relax or be immediately con- 
tracted again if an attempt is made to flex the limb. 

Finally the simulator cannot cause the loss of the knee-jerk and 
ankle clonus, which occurs after a severe epileptic attack. 

Prognosis. There is so much uncertainty about the course and 
termination of epilepsy that it is risky to assert an opinion. It may 
continue for years and the patient die of some other disease, such 
as pulmonary tuberculosis. ( )n the other hand it may suddenly de- 
velop into the dangerous and fatal condition of status. Some patients 
have attacks only once or twice a vear, others have them several 



212 THE NEURONIC DISEASES 

times a day. Often they appear in a series of several attacks during 
several days and then there will be none for a considerable time. 

It is not usual for the attacks to remain always of the same type. 
They tend as a rule to increase gradually in frequency and severity. 
In the more common form of the trouble the early attacks will be 
nocturnal and for that reason long unrecognized. They will then be 
discovered, by the roommate of the patient, and if he is not told of 
them, may continue as nocturnal and unknown to him. Usually, how- 
ever, attacks begin to appear in the daytime along with, or instead of, 
the nocturnal ones. They occur in the grand mal form about every 
two or three months and several times in the interval in the petit mal 
form. The minor fits may occur many times a day. 

There is always danger of accidental death in a seizure. Falls 
may result in fracture of the skull, severe and extensive burns, chok- 
ing and asphyxia by compression of the throat from extraordinary 
position, drowning and in a hundred other ways. 

Continuously nocturnal attacks are more dangerous than diurnal 
because they occur more frequently in feeble persons and overtake the 
individual when his vital forces are at their lowest. 

Though the immediate danger to life in epilepsy is not great, it is 
nevertheless a serious disease. While not so often killing the patient 
directly, it greatly jeopardizes his existence by the numerous fatal pos- 
sibilities it surrounds him with. Tuberculosis of the lungs 'terminates 
a considerable number of cases. Status epilepticus comes next as a 
cause of the fatal issue. About half of the cases of status die. 

Sudden death in a fit may be due to rupture of the heart, passage 
of food from the stomach into the trachea, asphyxia from position, 
sudden paralysis of the respiratory center and a prolonged tetanic con- 
vulsion. 

Spratling furnishes the following ratios : Of every one hundred 
epileptics who die, about four do so as the result of a single seizure ; 
twenty-four as the result of status ; twenty-four as the result of some 
lung disease, chiefly tuberculosis ; twelve as the result of accident in- 
cluding suffocation in bed ; ten as the result of some organic heart 
trouble: and about twenty-six from all other causes. 

Epilepsy, apart from its fatalities, always tends to shorten life. 
Early cases rarely pass beyond middle life. Later cases may continue 
into old age. De^th is not the worse thing to be dreaded by an epilep- 
tic. The terminal dementia ; the occasional maniacal attacks ; the out- 
bursts of emotion and rage with the commission of crime: are possi- 
bilities that death might beneficently forestall. The petit mal and 
psychic epilepsies are particularly to be regretted and guarded on this 
account. 

The question of the cure of epilepsy is just now undergoing a 
lively discussion. A hundred years ago or so the prognosis in this 
respect was much better than it is to-day. The cures were rated then 
even as high as fifteen per cent. Tt is not improbable that sympto- 
matic and other amenable forms of the disease entered into the making 
of these very favorable statistics. Perhaps more attention of a dis- 



THE NEURONIC DISEASES 213 

ciplinary and hygienic sort was given to the patient then than now. 
as the use of the bromides, undoubtedly overdone now, was unknown. 

On the other hand there are many to-day who regard epilepsy as 
an absolutely incurable disease. Such a pessimistic view is hardly 
justifiable. The term cure has a varied significance and while a res- 
toration back to a condition of perfect normality would perhaps be a 
Utopian dream, a cessation of the fits for years, and a gradual return 
to a better state of mind is certainly to be regarded in the light of a 
cure. 

If under the enlightened modern treatment of the disease with 
bromides and hygienic measures, and especially with the aid of the 
colonization method, all epileptics could be rigidly controlled, and if all 
the cases that improve, then wander away and never seek for further 
medical advice, could be gathered together, I am sure a set of tables 
could be constructed showing statistically a much more hopeful out- 
look for the cure of the disease. It certainly is not an absolutely in- 
curable trouble and the percentage of restorations, roughly and yet 
conservatively estimated under modern treatment as about five per 
cent, is enough to warrant the attempt in every case that offers the 
slightest degree of favorable indication. 

It would be a happy hit if we could always determine just which 
class of cases are the most amenable to treatment. Turner and oth- 
ers declare that senile epilepsy is essentially a tractable disease. The 
least favorable cases are those that begin under ten years of age. If 
arrest occurs between the fifteenth and twentieth years the outlook is 
particularly favorable. The chances for a cure then steadily decrease 
with the advancing' years but after thirty-five the intractable cases 
again begin to diminish. m 

Spratling says if there is a difference in the curability of the 
two sexes, he is inclined to think that it favors the male side. Contrary 
to the opinion held by some high authorities, the same author finds that 
the influence of the catamenia and marriage is not good but rather 
the reverse. The attacks have been unaltered in the least in most of 
the cases; in a few of them they have been increased in both frequency 
and severity. 

As is well known the grand mal type of the disease is more sus- 
ceptible of treatment than is the petit mal, and the diurnal than the 
11 .cturnal. Acquired and inherited mental weakness renders the out- 
look less hopeful in all forms of the trouble. The previous duration of 
the disease will also determine the patient's future chances. The re- 
moval of certain exciting causes, such as alcohol, syphilis, local mal- 
adies and reflex sources of irritation may, if done early, diminish or 
even stop entirely the attacks, with all further progress of the dis< 

Spontaneous recoveries have been reported but they are ><> rare 
as hardly to he taken into the consideration of the prognosis. The 
strong tendency of the disease is always to perpetuate itself. 

The probability of imbecility and idiocy should always he kept in 
mind in connection with infantile epilepsy. 

TREATMENT. Some one has uttered the paradox that the way 
to cure epilepsy is to stop the fits. This is one of those half-truths 



214 THE NEURONIC DISEASES 

which when lived strictly up to often do incalculable harm. Were 
the fits the whole of epilepsy, such an aphorism might establish good 
therapeutics. Unfortunately we are learning more and more that 
epilepsy is a deep-seated, continuous, obstinate disease of the brain, 
of which certain outbursts of a periodical sort constitute but one of 
many evidences. To stop the fits merely is, therefore, not the great- 
est good to be obtained from treatment. It does not in itself cure the 
disease. In some cases it has actually done harm. 

Every case of epilepsy, viewed from the therapeutic standpoint, 
consists of two elemental factors, the disease proper, and its violent 
exhibition in the fits. The latter are the outgrowth of the former and 
dependent upon it. By reacting upon a diseased and weakened nervous 
system, the frequent violence of the fits may undoubtedly increase the 
nervous weakness and underlying epileptogenous state. 

All treatment of epilepsy therefore must direct itself to checking 
the fits and to restoring the diseased nervous system. It must be both 
fundamental and symptomatic, general and specific, prophylactic and 
alterative — in a word it must attack the trouble at its source and it 
must restrain it in its violent outbursts. 

Any line of treatment that confines itself to one or the other of 
these two sides of the picture will surely fail of attaining the best re- 
sults. The administration of the bromides to suppress the convulsions, 
to the exclusion of all other treatment of the patient as a victim of a 
profound general disease, is as unscientific and illogical as it would be 
to neglect the fits entirely and to try and cure him by attacking the 
general underlying condition. 

The superior results of institutional and colonization treatment 
over those generally obtained in private practice are due to the fact 
that in the latter, for obvious reasons, medicinal control of the fits merely 
takes precedence over the general hygienic, pedagogic,, disciplinary and 
tonic measures, whereas in the former it is just the reverse. 

It is a platitude to state that the first step in the treatment of 
every case of epilepsy is to make a thorough search for, and remove, 
every possible source of irritation. This is absolutely necessary in 
every case no matter what may be its heredity, its previous duration 
or its type. Nothing that is abnormal about the patient, and that can 
be removed or remedied, should be allowed to pass. To mention all 
the possible abnormalities would require an enumeration practically of 
all the diseases, medical and surgical, to which the human body is 
liable. Every organ, every tissue, every function should be closely in- 
terrogated and if found to be wrong, should be righted as far as it 
is in the power of modern science to do so. When this is done the fits 
will diminish and ameliorate in a certain proportion of cases. This 
is the mirage, however, towards which many sincere and skillful in- 
vestigators have been beguiled when announcing to the world that 
epilepsy is due to certain organic peripheral defects and that they have 
cured it by removing those defects. 

Operations upon the eyes, nose and sexual organs have all been 
heralded as cures for the disease. Sooner or later, however, the fits 
have returned in spite of the operations, showing that the reputed 



THE NEURONIC DISEASES 21 5 

cure was nothing but a temporary relief, not even a permanent ameliora- 
tion. 

All hope of curing the disease by thus removing mere peripheral 
excitants shows a lamentable misconception of its true central patho- 
genic basis. The eye-strain, the nasal polyp, the tapeworm, the phimo- 
sis, the constipation, or any other abnormal condition, must be re- 
moved as promptly as possible. It will not cure the disease but it will 
remove possibly an excitant of an epileptic central nervous system and 
so cause a diminution in the number and severity of the fits. 

The basis of epilepsy is a cortical change. If there is no change in 
the cortex and the fits are but a sort of a Round-Robin-Hood reflex 
manifestation from a peripheral excitation, I regard the epileptiform 
phenomenon in such a state of affairs as physiological rather than 
pathological. It is not true epilepsy though it may be highly epilep- 
tiform. 

It is obvious that the proper wearing of glasses, the excision of 
old cicatrices, the extraction of an ulcerated tooth, will put a stop to 
the reflex convulsive phenomenon. Nay more, if done early it may 
thus even be said to cure epilepsy, in some few cases, prophylactically, 
for it is undoubtedly true that the continuation of such a severe form 
of reflex action does sometimes set up an epileptic habit in the cor- 
tical cells, which may go on to the development of the typical degen- 
erative condition which underlies the true disease. 

It is never a trivial matter therefore to remove these various ab- 
normalities in epilepsy; it is trivial to regard the amelioration caused 
by such removal as a cure of the disease. 

Where a patient can best be treated is a question that always pre- 
sents itself. This cannot be answered until after many factors have 
been taken into consideration. If the disease is of a light form and 
the patient's intelligence is good he may get along well enough at home. 
Cases that first appear in adult life, after the mind has developed, as 
a rule do not need removal from home so much as those that appear 
in childhood and in which the mind is likely to be most seriously af- 
fected. 

In general it may be said that most epileptics, young or old, are 
better off away from their old haunts and companionships where they 
are neglected, continually looked upon as peculiar and are able to 
constantly draw invidious comparisons between their own unfortunate 
state and that of their friends and relatives. Institutions and colonies, 
and private sanitaria, when properly conducted, afford the best re- 
treat for them. Here their food, exercise, bathing, work and amuse 
ments can be regulated and systematized while they themselves can 
be protected from doing themselves or others harm if an insane fit 
should suddenly overtake them. 

If insanity complicates the case, of course removal to an asylum : - 
absolutely imperative, and though the insanity may be only tempo- 
rary it is better for the patient to remain there in case it should un- 
expectedly reappear. Even the mentally weak epileptics are undoubt- 
edly better off in an institution. 

The absolute control of the patient by the physician is a sine qua 



2l6 THE NEURONIC DISEASES 

non to any degree of success in the treatment, and this alone estab- 
lishes the superiority of institution over home management. 

Colonies, such as those at Bielefeld, in Germany ; Chalfont, St. 
Peter, near London, and Craig Colony, at Sonyea in New York State, 
are growing in popular and scientific estimation. ■ The home-life, the 
preservation of his individuality, the absence of the competitions, ex- 
citements, allurements and comparisons incident to urban and subur- 
ban normal life, and the sympathetic companionship and uniformity 
of avocations here secured cannot but exert a better influence upon the 
patient. His invalidism is less emphasized in the midst of such sur- 
roundings and his entire mode of life and treatment is under closer 
supervision. He is educated intellectually and physically, trained in 
the use of tools, set to do attractive tasks, and in every way encour- 
aged to regard himself as a useful and responsible member of the com- 
munity. This is wholesome upon the mind and so checks one of the 
saddest possibilities of epilepsy, namely, the mental deterioration. 

All epileptics need outdoor exercise. This is forcibly demon- 
strated, as Spratling says, by the records at Craig Colony, showing a 
less aggregate number of fits in summer than in winter, and less among 
men than among women. The outdoor exercise must be systematic and 
non-exhausting. Gardening, farming and tending cattle are espe- 
cially commendable. Mild, unemotional indoor games and occupa- 
tions are to be encouraged. 

Marriage, for obvious reasons, had better be discouraged among 
epileptics. Alcohol, tobacco and other dissipations can be given up. 
Spratling says that in some cases he has known smoking to bring a 
calm that the individual stood in need of. 

The dietary of an epileptic needs supervision in only a few par- 
ticulars. It should be simple and include the breadstuffs, milk, but- 
ter, fruits and cereals. Eggs are good but meats should be indulged 
in sparingly. Seeded berries, cake, pastry, condiments, pork, veal, 
ham and grease-fried foods, alcohol, tea and coffee, should be avoided. 
Regular meals and abundance of easily-digested food should be the 
rule. The stomach must not be overloaded. 

The omission of sodium chloride from the diet of the patient is 
the latest suggestion that seems to have proved beneficial in a larg*e 
number of cases. 

Climatic, hydrotherapeutic and electrical treatment can only affect 
the disease indirectly by upbuilding the general constitution. 

The medicinal treatment of epilepsy is very old and consequently 
boasts of a long list of remedies. Some of these are still used, though 
they are probably without influence upon the disease. Others mod- 
ify the disease indirectly either by acting as general tonics, suppress- 
ing the nervous excitability, or influencing the circulation. We have 
no remedy that will make over the degenerated cortical cells into nor- 
mal healthy organs. We can only affect their abnormal function, ap- 
parently not their histological structure. If. however, we can check 
their excessive expenditure of nerve force, we may be able to put them 
in such a state of quietude that they can catch up, as it were, in their 
self-nutritive processes and this in the course of time will restore them 



THE NEURONIC DISEASES 2IJ 

to a more or less normal condition histologically. It is only within re- 
cent years that the medicinal treatment of epilepsy has been correctlv 
appreciated, put upon a sound basis and afforded the most desirable 
results. 

As we are ignorant of the minute cellular changes upon which the 
epileptic phenomena depend, and as we only know that certain medic- 
inal agents seem to have the power of suppressing these phenomena, 
without knowing how they do it, their administration is regulated by 
the changes produced by them on the fits. In other words the medic- 
inal treatment of epilepsy is purely a symptomatic treatment, and 
the chief end of our efforts by these means is the suppression or 
diminution of the paroxysms. 

This statement of course does not apply to the use of general ton- 
ics like iron and quinine, nor to the use of remedies directed against 
particular constitutional conditions like syphilis, malaria, alcoholism, 
and other forms of intoxication and infection. And it will have to be 
modified if in the future it should be discovered that toxaemia plays 
the chief role in the disease, and serotherapy is established on a posi- 
tive scientific basis. 

In the control of the paroxysms sometimes immediate measures 
are wholly or partially successful. These of course are only appli- 
cable when there is a distinct aura of sufficient duration. Patients 
can carry about with them the small glass pearls, each containing three 
minims of nitrite of amyl, and when they feel an attack coming on, 
can quickly break one in the handkerchief and inhale the vapor. A 
small bottle containing a bit of cotton saturated with the nitrite can 
be quickly uncorked and the contents inhaled. It is supposed that this 
flushes the brain with a rush of blood, or at least relaxes the vasomotor 
spasm of the cerebral circulation upon which the paroxysm is hypo- 
thetically believed by some to depend. At all events it is so often ef- 
fective in abating attacks that it is wise for all patients to carry the 
drug and use it if they have time to do so. 

When the aura begins in a limb, an old and sometimes success- 
ful manoeuvre is to suddenly constrict the limb with a tight band. 
Many patients wear a strap continuously and so arranged that they 
can quickly draw it tight themselves. Strong flexion, extension or 
traction on a limb may be tried. 

Cutaneous stimulation with a dash of cold water, tickling, pinch- 
ing, rubbing and slapping is also sometimes available. Two or more 
epileptics can travel together and serve each other in this way. 

Chloral hydrate in hypnotic dosage, or a teaspoonful of common 
salt, may abort an attack. 

According to Fancher and Spratling a few case.- have been checked 
by the hypodermatic injection of 1-10 or 1-15 of a grain of apomor- 
phine. Vomiting will probably follow but that often occurs in epilepsy. 

Brown-Sequard, Bravais, llirt and Buzzard have attempted to 
abort the seizures by maintaining a permanent blister about the limb. 

It is always to hv remembered that many patients are better for 
having a seizure, and hence it is not always desirable to check it. If 



2l8 THE NEURONIC DISEASES 

they are somnolent, stupid, subject to headache and distressed in feel- 
ing after the abortion of the fit, it had better not be checked next time. 

In all cases it may be said that the aborting of attacks does not 
modify the disease, and is only commendable on the grounds of per- 
sonal comfort and the avoidance of the possible accidents. These, how- 
ever, are reduced to a minimum by having the patient under constant 
surveillance. 

When the attack has occurred there is not much to be done, ex- 
cept to guard against accidents. The clothing should be loosened, a 
piece of cork or rolled-up rag should be placed between the teeth to 
prevent biting of the tongue, the general attitude should be arranged 
so that if vomiting occurs food will not slip into the trachea, and the 
patient placed where he can sleep after the paroxysm is past. 

In status epilepticus rectal injections of chloral hydrate, forty- 
five to sixty grains, or amylen hydrate, five to eight grains, should be 
tried. Morphine is generally useless though it may be used in combi- 
nations. 

The following emergency formula is highly recommended for 
status by Clark : 

^ Tr. opii deoderat. m. v. 

Potass, bromid. gr. xxv. 

Chloral hydrat. gr. xx. 

Liq. morph. sulph. (U. S. 5j. 

Sig. — One dose ; repeat in two hours if necessary. 

If these remedies fail to modify the attack, bloodletting should be 
resorted to. The condition is desperate and .the remedy must necessa- 
rily be heroic. 

Of all the remedies employed to control the fits the bromides still 
continue to enjoy the highest favor. They were introduced as anti- 
epileptic remedies by Laycock over half a century ago, and though 
they have been much abused and even when carefully employed do 
not constitute an ideal therapy, they are the best medicinal agents that 
we possess. Their mode of action is quite unknown and their ad- 
ministration must always be empirical. On this account there is even 
to-day, after these long years of trial, much diversity of opinion as 
to how they should be used. 

As drug treatment is necessarily so predominant in the home 
treatment of epilepsy, the abuse of the bromides is observed more in 
private than in institutional practice. As a rule the remedy is given 
in too large quantities, it is pushed after it has demonstrated its in- 
effectiveness, and it is not administered in proper time relationship to 
the expected paroxvsm. Moreover, when it is found to be effective 
and well borne it is not continued long enough. 

There are a number of bromide salts that are available, though in 
my own experience, as well as in that of others, the potassium salt is 
in the long run the most useful. Some physicians prefer the use of 



THE NEURONIC DISEASES 2IQ 

■a. single salt, others a combination of two or three of them. The 
potassium, sodium, ammonium and lithium bromides may be used in 
this way, the relative dosage varying according to the idiosyncrasy of 
the patient and the predilection of the prescriber. Strontium bromide 
is said to disturb the stomach the least. Calcium bromide, gold bro- 
mide, zinc bromide, bromium and camphor monobromate are other 
-eligible preparations that may be tried when those first mentioned fail. 
As a rule these will fail, too, but in a disease that is so obstinate one 
is glad at times to have something to ring the changes on. 

The bromides may be used alone or in combination with other 
Temedies to be mentioned. 

Two cardinal rules are to be observed when they are resorted to. 
The one is to use them in the best way, and in only such quantity as 
will check the fit. The other is to continue them, when found to be 
.effective, for a year or more in spite of the absence of all symptoms. 

The average case takes from a dram to a dram and a half a daw 
This may be administered in several small doses or, better still, in one 
large dose timed so that the maximum effect of the bromide will cor- 
respond with the hour of the expected fit. 

When stopping the use of the bromides it is never safe to with- 
draw them all at once; this has occasionally precipitated a condition 
of status. 

Xo rule can be set down for the administration of these prepara- 
tions, as the greatest success is obtained in studying carefully their 
effect upon each individual case. 

Dilute them largely with water ; do not administer them within 
an hour before or after meals; give ihem to the point of tolerance; 
prepare the largest dose about five or six hours before the expected 
fit, whether it be nocturnal or diurnal, continue the remedy for one or 
two years ; withdraw it gradually ; and employ it with the expectation 
of the best results in grand tnal, and the least favorable results in petit 
mal and psychic epilepsy. 

Such are the main points to be remembered. 

Certain accidents are to be avoided in the use of the bromides. Of 
these the gastric disturbances and the facial acne are especially unfor- 
tunate. Sometimes these can be avoided by the administration of 
iron and arsenic during the course of the bromides. Mitchell has seen 
irritability, melancholia at menstruation, bad temper, suicidal or hom- 
icidal tendencies and temporary delusions produced by them. They 
do undoubtedly depress the mental faculties; so does the disease for 
which they are administered. It is not always assumable, therefore, 
that every case of mental deterioration during a course of bromism i.^ 
the result of the medicine. 

In the hypochlorization method of Toulouse and Richet the pa- 
tient's food is salted with bromide of sodium instead of chloride of 
sodium. It is said that ten grains of the salt given in this wa\ is 
equal in effect to twenty grains given in the usual way. The method 
is worth trying in some cases, though it is not always successful. 

Spratling commends highly bromipin, especially in feeble or 



220 THE NEURONIC DISEASES 

asthenic cases, in children, and for hypodermic use in status epilepticus- 
For ordinary administration he recommends the following formula : 

1$ Bromipin giv. 

Syrup, simp. giv. 

Spts. menth. pip. 3iv. 

Mucil. acacise ad o xv J- 

Sig. — One to one and a half ounces, for adults, three times a day r 

after meals. 

It does not affect the gastro-intestinal canal ; does not produce 
acne;, and does not cause abscess when given hypodermically. 

Opium has long been tried in the treatment of epilepsy but it 
has not retained popular favor. Lately it has been used again but in 
combination. In 1893 Flechsig formulated a treatment with opium 
and the bromides. For six weeks mild opium narcosis is maintained. 
The drug is then suddenly withdrawn and the bromide substituted in 
doses of 120 to 130 grains daily, and continued for two months. The 
latter is then gradually reduced and maintained at about 30 grains a 
day. 

The plan is of doubtful efficacy and its dangers are not insignifi- 
cant. In my own experience, though limited, it was not superior to- 
the use of the bromides alone. 

After the bromides there are two remedies about equally divided 
in popular favor. They are atropine and borax. Either one may be 
given in combination with the bromides. Small doses are to be em- 
ployed in the beginning, and gradually increased until tolerance is ob- 
tained. Both may be continued for a long time. The extract of bella- 
donna may be used instead of the alkaloid. The conjunctivitis and 
eczema that are liable to occur after the prolonged use of borax are 
best combated with arsenic. Its cumulative tendency seems to give 
rise to persistent attacks of furunculosis and this militates somewhat 
against its use. 

The bromides have also been used in conjunction with antipyrin, 
digitalis, adonis vernalis and chloral hydrate. 

Ethylene bromide in doses of one or two minims two or three times 
a day, in emulsion or capsule, seems to have been effective in a number 
of cases in controlling the fits. 

Amylene hydrate, in from a half to two dram doses daily, was 
extensively tried by Weber. Only five per cent, of the cases responded 
favorably to it, and these were disturbed in general health and made 
drowsy, sluggish and dyspeptic by it. It may sometimes act better 
than chloral in cases of status epilepticus. 

Nitroglycerin in minute, frequently repeated doses may act happily 
in senile epilepsy where there is marked arteriosclerosis. 

Zinc is a historical but not much used remedy nowadays. Ure- 
thane in doses of twenty to forty-rive grains has been commended by 
Jacobi and Spratling. Chloretone acts somewhat like the Flechsig 
treatment. According to Weeks, it should be pushed as rapidly as 
possible. About six grains three times a day is the proper dose for 



THE NEURONIC DISEASES 221 

prolonged usage. Solanum carolinense (fluid extract, o l / 2 to 5j t. i. d.), 
and simulo (tincture 5ij to oiij t. i. d.), have had their advocates. They 
are useful sometimes when the bromides cannot be tolerated, are com- 
paratively harmless and are therefore always open to trial. Trional has 
been tested and found to be useless. The coal tar derivatives, anti- 
pyrine, phenacetine and acetanilid, affect the heart and fail to affect 
the epilepsy. 

In a small proportion of cases continuous chloroform narcosis 
may be a dernier ressort. It cannot be relied upon, however. The 
employment of electricity, hydrctherapeutics and other general meas- 
ures, except for their general constitutional effect, shows a want of 
appreciation of the true nature of epilepsy. 

The valerianates, aniline sulphate, silver nitrate, asafcetida, calabar 
bean, camphor, cannabis indica, chloralamid, conium, copper-am- 
monio-sulphate. duboisine, gaduol, hyoscyamine, ignatia, strychnia. 
lobelia, paraldehyde, phosphorus, physostigma, picrotoxin, rue, san- 
tonin, sodium fluoride, spermine, stramonium tincture, sulphonal. 
sumbul and many others constitute a list of remedies that may be tried 
when the usual medicines fail. These will doubtless fail, too, but their 
administration may be useful for the constitutional, tonic or psychic 
effect while other more general measures are being put into force. 

Bacterial products, serum therapy and other measures to produce 
immunity and to combat the toxaemia are being experimented with by 
those who believe in the intoxication and autointoxication theory of 
the disease. So far the results have not been very encouraging. 

Surgery for the relief of epilepsy is more especially applicable in 
so-called symptomatic epilepsy. Cranial depressions, spicuke of bone, 
old cicatrices, cortical cysts, meningeal thickenings and other cranial 
and cerebral abnormalities should always lead to the question of 
trephining. The draining of an abscess may put a stop to the disease. 
I have seen the fits stopped for a long time by the simple operation of 
trephining in a case of multiple abscess discovered during the operation. 

According to Sachs and Gerster symptomatic epilepsies that have 
existed for more than three years do not offer a very promising out- 
look from operative procedure. The more recent the injury the better 
the prospect for ultimate recovery from surgery. 

Surgical measures are often called for in the removal of some 
peripheral source of irritation that may be keeping up a reflex type of 
the disease. I have elsewhere stated that all such excitants must be 
removed, if possible, in even' case. 

The use of the seton in the nuchal region, the ligation of the 
carotid and vertebral arteries and the extirpation of the sympathetic 
ganglia, are among the historical and curious relics of the surgical 
treatment of epilepsy. 

HEMICRANIA. MIGRAINE. 

This is a paroxysmal neurosis, periodical and epileptiform in char- 
acter, in which headache and other special sensory symptoms constitute 

the prominent feature. If it were a mere headache, its classification 



222 



THE NEURONIC DISEASES 



would fall in the following section and be subject to the same criticism 
made there in regard to all forms of cephalalgia. Some authorities 
regard it as a special disease entity. -In deference to their views and on 
account of the uncertainty of our knowledge as to its exact pathology,, 
it may be wise for awhile yet to devote to its discussion a special chap- 
ter. I place it here, however, because, as I will show later on, I believe 
it is most intimately related to epilepsy, is possibly a sensory epileptic 
equivalent of a special type and should be considered under the general 
head of epilepsy. 

Etiology. — No fact is more patent in the etiology of migraine than 
that it is an inherited trouble. The inheritance may run through several 
generations and be either direct or indirect. How frequently we are 
told by the victims of this disease that their father or grandfather suf- 
fered from similar attacks of headache ! They often volunteer the in- 
formation that they have a brother or a sister who is also afflicted with 
it. The maternal ancestry may also have been subject to it, though 
it has seemed to me that direct heredity was less prominent on the 
maternal than on the paternal side. Gowers asserts that in more than 
half the cases distinct heredity can be traced and that usually it is direct. 
An indirect inheritance is not uncommon and usually consists of a 
strong neuropathic taint. This may come from either side of the house 
and may have sprung out of ancestral dissipation, excessive mental 
work or some related nervous disease. Epilepsy, hysteria, mild psycho- 
ses, neuralgia, gout, asthma, paroxysmal cardiac troubles are among 
the diseases noted in the family history. 

Given this inherited neuropathic constitution, it is obvious how the 
exciting causes of migraine may be both numerous and varied. 

All unwonted strains, whether mental, nervous or physical, may 
start up an attack. A great emotion, fright, prolonged mental labor, 
anxiety and worry will cause it. One of the worst sufferers I ever 
treated was a young girl, whose father, now dead, had had the disease, 
who was attempting to finish a college course during the absence of 
her lover to whom she expected soon to be married, and with the con- 
tinual presence of her mother, who was an ignorant, self-opinionated, 
nagging woman. Only the strictest seclusion in a hospital for a time 
saved the girl from what almost threatened to be complete mental 
breakdown. 

Peripheral reflex excitants may provoke an exacerbation of the 
disease. Masturbation, coitus, hypertrophy of the nasal mucous mem- 
brane and working in overheated rooms have been blamed for it. 

Autointoxication, with or without obstipation, is believed by many 
to be a most important factor in the etiology. 

Peripheral diseases and deformities may well play a role in exciting 
it. Eye-strain in one predisposed to the trouble is just as much a cause, 
no more, no less, than might be disease of the sexual organs. Anaemia, 
overlactation and other depressing influences will aggravate it. It 
has occurred in connection with diabetes and chronic nephritis. 

The similarity between the etiology of migraine and that of epilepsy 
is very impressive. It is an inherited neuropathic condition, a high 
degree of nervous instability upon which an innumerable list of ex- 



THE NEURONIC DISEASES 223 

citants, chemical, physical and functional, operates to provoke an 
exacerbation or paroxysm. 

Weir Mitchell has lately compared the atmospheric storm curve 
with the headache curve and finds a relationship. March and April are 
the worst months, October and February the best. 

Pathology axd Pathogenesis. — There are no discoverable char- 
acteristic anatomical changes in hemicrania. This fact stands as an 
unanswerable argument against all theories in which this neurosis is 
attributed always and solely to a reflex irritation. If hemicrania is 
due to eye-strain, then eye-strain must always be found, with the ac- 
companying anatomical defect, in all cases of the disease. 

As a matter of fact, there is no pathology known. A neuropathic 
condition of the central nervous system is assumed on account of the 
heredity and other suggestive phenomena, while the exciting anatomical 
and physiological causes of the outbreaks of the disease are both obvi- 
ous and numerous. 

\\ "here so little is known, theorizing is always rife. Of all the 
pathogenetic explanations of the disease, two only are worthy of special 
consideration. The first is that hemicrania is but a form of epilepsy ; 
the other is that it is the expression of a vasomotor disturbance due 
to disease of the sympathetic nervous apparatus. 

It seems to me that if any reliance is to be placed upon compari- 
sons at all, the etiology, symptoms, course, occasional complications 
and other manifestations associated with migraine point most clearly 
to its relationship with epilepsy. The heredity in the disease, the de- 
pendence of the outbreaks upon exciting causes, the periodicity that 
occurs in these outbreaks, their onset, progression, sudden termination 
and sequelae are so strongly epileptiform that if they are not epilepsy, 
no two phenomena ever came so near being alike while yet being unlike. 
The only difference between epilepsy and hemicrania is that the former 
is characterized by prominent motor symptoms, while the latter is 
almost wholly sensory. This, however, is only an apparent and not a 
real difference. 

In epilepsy of the petit mal and psychic type motor symptoms are 
often wanting, while in hemicrania it sometimes happens that slight 
motor phenomena can be observed. To be sure, the mental disturbance 
is the cardinal feature in all epilepsies ; but in hemicrania the mind is 
very often seriously affected. This is seen in the amnesia, aboulia, 
aphasia, irritability, want of attention and stupor, which, however, 
never or very rarely passes into the complete unconsciousness observed 
in epileptic fits. The sensory character of migraine is, if anything", 
confirmatory in part of its epileptic nature in view of the more recent 
conception of the pathogenesis of epilepsy. The latter is by most 
modern pathologists now believed to be primarily a sensory disease. 
The sensory elements of the cortex have been found to show certain 
chromatolytic changes. A toxic degenerative condition attacking these 
sensory elements causes them to manifest the early signs, aura, etc., 
of the fit. Their close connection with the motor elements is the 
explanation of the severe secondary spasms and convulsions. The 



224 



THE NEURONIC DISEASES 



severity and wide extent of the nerve storm accounts for the profound 
coma. 

In hemicrania a somewhat similar succession of events takes place, 
but milder in degree. There are the sensory prodromic intimations, 
then the nervous explosion, which, however, does not overflow into the 
motor elements to the same extent that it does in grand mal, and 
finally the sudden cessation with more or less lingering sequelae. 

The outward exhibition of the two diseases being thus so much 
alike, it is but fair to assume that there is a similarity in the underlying 
pathology, whatever that may ultimately prove to be. In epilepsy 
the process is generally accepted to be located in the cortex. In mi- 
graine it is probably cortical also. 

On account of the prominence of the headache and of the gastric 
symptoms, some hold that the maximum foci of the disturbance are 
localized in the primary centers or ganglia of the trigeminal and 
pneumogastric nerves. This may be true, but on account of the eye 
symptoms, mental disturbances, aphasia and occasional motor phe- 
nomena we must still believe that the neurosis is in large part, if not 
wholly, a cortical trouble. 

One way, and perhaps the best way for the present, to express the 
relationship between the two diseases is to say that migraine is an 
epileptic equivalent. 

Under the head of epilepsy will be found a discussion of these 
so-called equivalents. 

Of all the explanations of migraine, the one that allies it to epilepsy 
is to-day the most generally accepted. It has the support of Liveing, 
Gowers and many others. 

The other popular theory of the disease is that a spasm of the 
cerebral arteries causes it. Whytt and Du Bois Reymond were the 
leading sponsors of this explanation. Mollendorf and others, on the 
other hand, urged that vascular dilatation rather than contraction was 
the basis of the trouble. Many writers, like Latham and Eulenburg, 
think that both spasm and dilatation of the blood vessels are the cause 
of the disease, and, with most followers of this theory, assign the pri- 
mary cause of the vascular trouble to the sympathetic nervous system. 
Latham thinks that the early symptoms are due to vascular contrac- 
tion, the later, and especially the headache, to dilatation. Eulenburg 
and others make two leading types of the disease, which they have 
denominated the sympathetico-tonic and sympathetico-paralvtic re- 
spectively. 

The weakness of this vascular theory is that the basis for it con- 
sists in the mere appearance of certain accessible arteries during an 
attack. It assumes that the same thing is occurring in the intracranial 
that is observed in the extracranial circulation ; that this is a cause 
rather than an effect of the disease, and that it is dependent upon some 
hypothetical change in the sympathetic nervous apparatus. In addition 
to assuming so much, the theory is not founded upon a single post 
mortem finding that would lend it color or support. Furthermore, it 
does not account for the remarkable similarity between the general 



e>> 



THE NEURONIC DISEASES 225 

symptomatology and etiology of migraine and epilepsy, unless it is 
likewise adopted as the explanation of the latter disease. 

It seems to me clear that as migraine is so closely related to epi- 
lepsy, all theories that are advanced to explain the former disease 
must be employed to explain the latter. This the vascular theory does 
not do, and it is therefore inadequate to explain the nature of migraine. 

Migraine is a primary neurosis, of which the sudden vascular 
derangement is one of the manifestations. 

The exact primary seat of the neurotic storm is not yet determined, 
though most of the indications point to the sensory centers of the 
cerebral cortex. 

Symptoms. — Very many cases of migraine have premonitions of 
an oncoming attack. In others the onset is sudden and abrupt, some- 
times awakening the patient out of his sleep at night. The premoni- 
tory symptoms are not unlike the premonitory signs and aura that 
precede an epileptic fit. For a day or two, or several hours, the patient 
will feel tired, listless and indifferent. Somnolence and a fullness of 
the head are complained of. Sometimes there is unusual mental bril- 
liancy, with a surprising activity of memory, imagination and intel- 
lection. As a rule, however, the apathetic condition, with yawning 
inability to fix the attention, vertigo and depression obtains. An ab 
normal hunger or indifference to food, with slight feeling of nausea and 
cardiac palpitation, have been spoken of by patients before the onset of 
the headache. Immediately before an attack other patients experience 
visual disturbance, as, for instance, spots flying before the eyes, flashes 
of color, rainbow formations, star-like fortification figures, hallucina- 
tions of animals and strange creatures. Sometimes the visual field 
slowly increases or decreases, grows dark or light, becomes dark in 
segments, with transient hemianopsia and scotoma. A blurring of the 
vision more frequently occurs. Hippus or alternate contraction and 
dilatation of the pupil has been seen. 

The other special senses are only rarely subject to these aura-. 
Tinnitus aurium, parosmia, numbness of the mucous membrane of the 
mouth, have been noted. 

Paraesthesia and, more rarely, cramps and spasms have appeare I 
in the upper extremities just before an attack. 

Transient aphasia, more particularly of the amnesic type, has 
sometimes been premonitory of the headache. 

When these sensory premonitory manifestations arc marked, it 
its that the succeeding headache is less severe and less definitely 
localized than when they are slight or absent entirely. There is 
absolute rule about this, however. Some patients have actually had 
these aurse without the appearance of the headache at all. 

An attack of migraine or paroxysm of the disease presents a cer- 
tain constant clinical picture, the details of which are subject to much 
modification. 

Soon after the appearance of the premonitory symptoms, and 
letimes even without them, a headache occurs abruptly or gradually, 

lily increases to a climax, where it remain- several hours, accom- 
panied by certain sensory, motor and psychic manifestations, and then 



226 THE NEURONIC DISEASES 

rapidly disappears with usually an attack of vomiting, leaving the 
patient exhausted, sleepy and depressed. 

It is to be noted that the attacks are more or less periodical and 
paroxysmal ; that they pretty closely resemble one another always in 
the same patient ; and that they are separated by intervals of apparent 
perfect health. 

The headache is their prominent, but not their only, symptom. 

They are often provoked by overexertion, indiscretions in eating, 
mental excitement and unusual use of the eyes. Sometimes they come 
apparently unprovoked. 

Paroxysmal headache with vomiting, visual disturbances and other 
less constant symptoms, appearing rather abruptly, rising to a maxi- 
mum of intensity, remaining there a certain number of hours, and then 
abruptly vanishing, constitutes the clinical picture, in brief, of an attack 
of migraine. 

As the minutiae of this picture are subject to much variation, I 
will now discuss them a little more in detail. 

Though it has given the name to the disease because it is so 
constant and prominent, the headache is not by any means its sole 
or most important symptom. In rare instances it is entirely absent, 
and in all cases the patient has become so accustomed to it that though 
it causes him the most discomfort, it does not alarm him so much as 
some of the sensory, motor and psychic phenomena that accompany it. 

This is to be remembered both on account of the proper concep- 
tion of the disease and its proper management. 

Hitherto in the profession, and even yet to a large extent among 
the laity, the headache has been regarded as the cardinal feature of the 
disease, and in a way the cause of all its other manifestations. 

The disappearance of the cephalalgia synchronously with an at- 
tack of vomiting and vertigo has fixed the impression in the minds of 
the people that the liver is somehow the cause of the headache, and 
that if the vomiting of bile can only be induced, the headache must of 
necessity vanish. They, therefore, commonly speak of migraine as 
"bilious sick headache," totally ignorant of the fact that both the head- 
ache and the so-called bilious manifestations are synchronous 
phenomena depending upon the same neurotic process. 

In a general way it may be said that the more pronounced the 
cephalalgia is the less obvious will be the other special sensory and 
motor symptoms. When the latter are marked, the headache is apt 
to be of a minor degree of severity. 

The character of migrainous headache is quite distinctive. As I 
have intimated, it appears rather suddenly, but develops gradually. 
Sometimes it bursts forth in all its excruciating intensity at the very 
beginning. It does not fluctuate, but continues steadily, after it has 
reached its climax, for a day usually — sometimes only a few hours, at 
other times for two or three days — and then rapidly vanishes. It is 
generally a unilateral headache, the seat of its maximum intensity be- 
ing in the temporal region. After remaining awhile in one temple it 
may cease, only to reappear in the other temple. It may extend from 
one temple over the front of the brow or across the top of the head to 



THE NEURONIC DISEASES 22^ 

the other temple. Not infrequently the pain starts in the occipital 
region, extends forward to the supraorbital region, or down the neck, 
even into the arm. In the same patient it usually occupies the same 
locality and extends in the same general direction with each succeed- 
ing attack. Occasionally it always appears in one way during a cer- 
tain period of life, and in another way during another period. Its 
localization, steadiness, intensity and paroxysmal character are among 
its striking qualities. 

The pain itself is of a burning, boring sort ; more often just a dull, 
incessant, sickening ache. At first it may seem to be superficial, but 
later on it feels deep in the cranium. Percussion aggravates it, as 
well as light, noise, or any peripheral irritation. Mere pressure does 
not increase it, but rather affords some relief. Movement, jars and 
other slight disturbances seem to awaken it to renewed intensity. The 
patient therefore instinctively seeks a couch in a dark and silent room 
and is irritable with those who disturb him even with their good offices. 
The skin of the head may be hypersesthetic, and while the pain is on 
al! the nerves of the body, but especially the fifth nerve, have their 
sensibility highly exalted. Hence the patient is in a wretched state, 
limp, irritable, excited or stuporous, and indifferent to those about him 
and their attentions. Frequent experiences have taught many of the 
victims of this disease to bear it in patience and to await in seclusion 
its early termination. 

There are all degrees of the headache, though as a symptom it is 
more or less always present. It may continue to be the chief mani- 
festation of the disease throughout life, or it may suddenly cease, to 
be replaced by some other neurosis. Two sisters whom I saw suffered 
all their lives with asthmatic attacks, except one of them who twelve 
years ago began having attacks of migraine in place of those of the 
asthmatic neurosis. 

It sometimes happens that the headaches stop and epileptic seiz- 
ures begin. 

I have seen the headaches alternate with hysterical outbreaks, and 
other spasmodic conditions. 

The headaches never occur alone, a fact which more than any- 
thing else indicates the protean and extensive nature of the disease. 

Next in frequency to the headache, and usually accompanying it, 
arc the gastric phenomena. These consist of anorexia, acute indie 
tion, nausea, retching and vomiting. That not one of these is in direct 
relation to the headache is shown by the fact that the latter is in no 
way modified by them when they occur early in its course. Distress in 
the stomach may precede the head pain, occur when it is at its height, 
or appear only when the latter is beginning to wane. Usually then 
some anorexia and nausea from the beginning of the attack, and then 
it the end violent retching and even vomiting of bile accompanies the 
sation of the headache. If food is taken it fails to digest and comes 
up with the retching. This symptom causes great distress and prostra- 
tion sometimes and is generally the terminal manifestation of the par- 
oxysm. Sleep and quietude follow it. 



228 THE NEURONIC DISEASES 

In some cases there may be diarrhoea and polyuria towards the end 
of the attack. 

In about half of the cases there is some visual disturbance. This 
assumes a great variety of forms and usually indicates trouble in the 
occipital cortex. When both eyes are affected, the phenomenon usually 
occurs in similar parts of the visual fields. Complete or partial hemi- 
anopsia may occur or the vision in one or both eyes may be blurred. 
Flashes of light, star formations, highly colored zigzag lines or fortifi- 
cation figures are not uncommon. Actual hallucinations of animals 
have been observed. Moving phenomena are particularly frequent. 
Spots float across the field of vision, objects approach and recede, 
diminish and grow large, or become alternately brilliantly luminous 
and dark. Central scotoma ta have been seen. In rare instances double 
vision has occurred. 

All of these manifestations may appear abruptly or come on 
gradually ; they may be more or less constant, though as a rule they 
come and go or change from one to the other in the course of the 
attack. 

The functional character of these troubles and their dependence 
upon the higher or cortical visual centers are obvious. With the 
headache and stomach troubles they complete the tripod that most 
frequently makes up the clinical picture of an attack of migraine. The 
other symptoms to be mentioned occur much more irregularly and in- 
frequently than these three. 

General sensation is affected in many patients in such a way as 
to clearly indicate a cortical functional trouble. Unilateral or bilateral 
paresthesia and even anaesthesia may occur in' the arms, rarely in the 
legs, in the face, mouth, throat and neighboring parts. Numbness, 
tingling, pins-and-needles, a feeling as of water flowing over the skin, 
hot and cold, are the more common cutaneous disturbances complained 
of. As with the aurae of epilepsy, these sensations sometimes travel 
up the arms in gradation or in skips, and then appear in the foot and 
travel up the leg. They rarely last longer than a few minutes. The 
tongue and fauces sometimes feel numb and may become actually 
anaesthetic. Paraesthesia of the limbs usually precedes in time paraes- 
thesia of the face and lips. When unilateral it is of the hemiplegic 
type, involving the same side in the face and limbs. These cutaneous 
disturbances are far less frequent than those of the sight. 

In very rare instances the other special senses have been affected. 
Tinnitus aurium, parosmia and alterations of taste are possible, but not 
common. Transient deafness in one ear, hallucinations of hearing and 
taste and other bizarre observations have been recorded. 

The motor symptoms are never prominent and are usually entire- 
ly unnoticeable. Slight weakness of the hemiplegic type may be ob- 
served in the limbs, or they may exhibit a certain degree of spasm. 
These motor manifestations, when present, appear on the opposite side 
from that of the headache. They are always associated with sensory 
symptoms and are exceedingly transient in duration. Cerebellar inco- 
ordination was observed in one case. 

The vasomotor symptoms are much more commonly observed. 



THE NEURONIC DISEASES 220, 

Usually there is an initial spasm of the facial blood vessels with pallor. 
This may continue through the attack. In other cases it is replaced by 
a congested and flushed condition. Pupillary changes, unilateral sweat- 
ing, oedema, redness of the conjunctives and retardation of the pulse are 
some of the occasional observations. These phenomena are usually 
bilateral, though they may be one-sided. They point clearly to implica- 
tion of the sympathetic nerves, but are neither constant enough nor 
sufficiently indicative of the intracranial circulation to found a theory 
of the disease upon the sympathetic nerve, as some have attempted 
to do. 

Aphasia of the amnesic variety, more rarely of the motor, is a 
symptom liable to appear. It is rarely complete and in a case observed 
by Oppenheim was combined with agraphia. Hemianopsia may be 
associated with the aphasia. Word-deafness, aphasia, etc., are seen 
in only a small percentage of cases in which the cephalalgia is left- 
sided. 

Giddiness and vertigo, with loss of equilibrium and nausea, are 
sometimes present. 

More or less psychosis occurs in all of the cases and it is not en- 
tirely due to the pain and distress experienced by the patient. It is a 
part of the paroxysmal phenomena. There may be slight excitement, 
irritability, intellectual brilliancy just before the onset. More often 
there is emotional depression, weakness of memory, lack of power of 
attention. There follows in some cases actual stupor or confusion, 
or transitory insanity with marked hallucinations. There is never com- 
plete unconsciousness, but a state of double consciousness has been 
seen. The memory may recall far-off events with extraordinary 
vividness. 

The general prostration caused by an attack of migraine is severe. 
Not only during the spell, but for some time after it, the patient is 
dull, apathetic and somnolent. At the climax of the paroxysm some- 
thing seems to suddenly give way. Vomiting suddenly occurs, the 
headache rapidly dies out, ptyalism, perspiration, profuse micturition 
occur and the patient passes into a profound sleep, from which he 
usually awakens some hours later refreshed and feeling quite well 
again. 

It is useless to attempt to establish types of the disease out of the 
many peculiar forms and combinations that the symptoms assume in 
different cases. The disease is always the same and mere prominence 
of this or that symptom does not alter it. 

In the larger number of cases there are present only cephalalgia 
and the gastric disturbance. When the disease occurs in children there 
may be some elevation of temperature, even to 102 or 103 degrees F. 

The sensory and other manifestations of the disease may rarely 
occur without the hemicrania. Eye symptoms, transient aphasia, 
paresthesia in the limbs may thus appear alone or in alternate attacks 
with the headache. Gowers cites a case in which for years the only 
symptom was a visual disturbance like that which usually precedes an 
attack of headache. At no time was there any pain. These ca 



230 THE NEURONIC DISEASES 

are exceedingly rare, but should be carefully studied and properly 
recognized. 

Some of these cases may belong to the class of hemicrani-al equiva- 
lents spoken of by Mobius. In this it is assumed that the disease is 
epileptiform and has equivalents just as ordinary epilepsy has. Among 
other equivalents noted are cardialgia, severe vertigo, gastroxynsis, 
circumscribed pains of a severe character in other parts of the body 
than the head, and attacks of hemiparesis. 

Temporary mania, mental confusion, dream states and melancholia 
have been seen in place of a migrainous attack. One of my patients 
would lock herself in her room, refuse food for days and do other 
strange things that led her own family to declare that she was insane, 
and to suggest her confinement in an asylum. During several months' 
treatment under my care in a private hospital she showed no signs of 
insanity, but had several unusually severe outbursts of headache. 

Mobius has made use of the occasional cases of constant hemi- 
crania to support the epileptic theory of the disease, calling these cases 
instances of status hemicranicus and comparing them to status epi- 
lepticus. 

Among the affections sometimes associated with hemicrania epi- 
lepsy stands prominent. Epileptiform attacks may mingle with those 
of headache or the latter may cease and be replaced by typical epilepsy. 
Writer's cramp and other occupation neuroses, as well as convulsive 
tic have been seen conjointly with it. Nearly all cases are somewhat 
either neurasthenic or hysteric. Both of these latter diseases may be 
developed out of the prolonged strain and suffering caused by the 
hemicranial attacks. As a rule, however, they are the product of the 
same neuropathic constitution that underlies the migraine. The im- 
portance of this fact is shown when one mistakenly attempts to treat 
a migrainous headache under the erroneous notion that it is but a 
symptom of the neurasthenia or hystero-neurasthenia that may be 
present. The latter may improve, but the hemicrania will probably 
remain. Disappointment will be then the portion of both the patient 
and physician. 

Diagnosis. — In fairly typical cases the diagnosis of migraine is 
easy. The points to be carefully noted are the heredity back of the dis- 
ease, the provocation of the attack by some unwonted strain, the pre- 
monitory symptoms, the somewhat abrupt onset of the unilateral head- 
ache, dragging in its train more or less marked visual and gastric dis- 
turbances, other sensory symptoms and even certain motor and 'vas- 
omotor manifestations. 

The comparatively brief duration of the attacks, their somewhat 
periodical and paroxysmal character and their sudden termination 
with severe vomiting should be carefully taken into consideration also. 
The association of the trouble with other neuroses, especially epilepsy, 
is quite confirmatory. 

However, other headaches are sometimes unilateral, paroxysmal, 
combined with other symptoms and in many ways may be confused 
with hemicrania. In these headaches assistance in making the diagno- 
sis must often be obtained solely from the other symptoms of the 



THE NEURONIC DISEASES 



231 



disease underlying the headache. The cephalalgia that often accom- 
panies hysteria, neurasthenia, uraemic poisoning, eye-strain, constipa- 
tion, etc., can thus be easily distinguished aside from their own char- 
acteristic features. 

In tumor of the brain the appearance of the fundus of the eve, 
the comparatively constant presence of the pain, the absence of the 
prodromes and peculiar visual disturbances of migraine, and, when 
present, the localization symptoms, will help to establish the diagnosis. 
The pulse may be retarded in migraine as it is in cerebral neoplasm, 
but in the former disease it is an exceptional symptom, while in the 
latter it is a common manifestation. 

On account of the elevation of the temperature migraine in child- 
hood may be mistaken for meningitis and other brain diseases. The 
paroxysmal character of the headache, the ancestral history and the 
absence of the usual objective signs that accompany these diseases 
will guide the diagnosis in the right direction. 

Petit inal may be overlooked as a case of hemicrania. The dis- 
tinction is sometimes a difficult one to make on account of the appar- 
ently close relationship between the two diseases. In ' epilepsy the 
visual aurae are not as prolonged as they are in hemicrania, the psychic 
manifestations are somewhat more prominent and the sensory symptoms 
are less noticeable. If the slightest convulsion occurs the diagnosis of 
epilepsy is of course assured. 

Tic douloureux appears in a particular nerve, the fifth, and has 
not the aurae, the eye symptoms, the general sensory manifestations of 
the hemicrania. 

Prognosis. — As inheritance is so important a factor in its etiology, 
migraine must be looked upon largely as of the nature of a congenital 
defect. This, of course, precludes the possibility of its complete eradi- 
cation. And yet it may cease suddenly at any time, though it is then 
likely to be replaced by some other form of neurosis or even psychosis. 
Most cases, however, continue having their paroxysms during all their 
lives. Cases that I have seen change have always been about the 
climacteric. In several instances I have seen migraine replace some 
previous neurosis about this period. 

The longer the disease has existed the smaller is the hope of its 
disappearance or even amelioration. The latter in many cases can be 
brought about by changing the patient's mode of life, environment and 
removing all possible causes of peripheral irritation. 

Hemicrania is practically incurable. The type of the disease in 
which the visual phenomena are especially prominent sometimes pre- 
cedes tabes dorsalis and dementia paralytica. When it is associated 
with hysteria, hystero-neurasthenia and other grave neuroses, especially 
epilepsy, the outlook is very unfavorable. Amelioration and the remote- 
possibility of a spontaneous cessation is about the besl sort of comfort 
we can hold out to these patients. 

The disease is decidedly chronic and in no way jeopardizes life, h- 
greatest danger, though that is not frequent, is its transition into 
epilepsy or insanity. 



232 THE NEURONIC DISEASES 

Treatment. — In undertaking the treatment of a case of hemi- 
crania, the first requisite is to remove every discoverable excitant of an 
attack. Many patients have discovered this fact for themselves and 
when presenting themselves to the physician for advice declare that 
they have carefully avoided all habits and acts that have initiated their 
attacks. Nevertheless it is always well to interrogate the patient closely 
in regard to his environment, his occupation, his dietary, his custom 
in regard to sleeping, bathing, exercising, in regard to his sexual life, 
his bowel functions and his brain work. Not a stone should be left 
unturned in this search. Proper corrections, of course, should be made 
where errors and excesses are found in the habits and manner of living. 
As migraine is in many cases a reflex disease, the patient's body should 
be thoroughly examined for physical and functional defects. The eyes 
may be defective in one case ; the nasal passages obstructed in another. 
An enlarged tonsil or a mastoiditis may be causing the trouble. 
Anaemia may be present, or there may be some latent renal disease. 
The very multiplicity of the exciting causes of migraine, and their 
elusive character in so many of the cases, urge upon the diagnostician 
unusual care and thoroughness in his search for them. Their removal, 
of course, is a sine qua non to all further treatment of the case. When 
this is done many cases will undergo marked amelioration and some 
will be absolutely cured. 

As the neuropathic instability frequently continues in such cases, 
other existing causes may arise and provoke the attacks anew. Those 
who vainly attribute migraine to these peripheral causes alone do not 
have a proper conception of the disease and are disappointed when 
there is a return of the headaches in some of the cases in which the 
supposed existing cause has been carefully removed. 

All discoverable causes having thus been removed as far as possi- 
ble, there should be an effort made to combat the disease by continuous, 
prolonged, constitutional treatment. 

The dietary should be regulated and rendered as bland and nour- 
ishing as possible. A purely vegetarian diet has modified some cases. 
Stimulants, condiments, fats and rich pastry had better be avoided. 
Tea and coffee are sometimes harmful. Milk diet is commendable, 
though a large percentage of these cases declare they cannot take 
milk. I have found this to be due largely to the psychic impression 
that biliousness, which they think they suffer from in their attacks, 
is somehow associated with the ingestion of milk. I nevertheless in- 
sist upon their taking the milk, in small, frequent quantities, and have 
more than once overcome the prejudice. 

I urge these patients to drink abundantly of pure water at all 
times. As constipation is not uncommon, some natural water with 
cathartic properties, like Carlsbad, Hunyadi, Friedreichshalle, is to 
be used more or less regularly before breakfast. The general health 
should be built up if necessary. Arsenic and iron and other tonics 
should be given if the state of the blood and organs calls for them. 
Hydrotherapy, mechanicotherapy, massage, gymnastics and electricity 
may all be advantageously employed with this end in view. A change 
of climate and a sojourn in the mountains, or by the seashore, may 



THE NEURONIC DISEASES 233 

so alter the general state of ill-health as to cause a marked ameliora- 
tion in the migrainous attacks. 

For the disease of hemicrania, like epilepsy, we have no specific 
medication. The prolonged administration of some remedies, however, 
has resulted in a number of complete and partial successes. Of these 
remedies arsenic, nitroglycerin and the bromides head the list. In my 
own experience arsenic has seemed to be the most successful. It very 
often fails, however. Any form of arsenic may be used, though arseni- 
ous acid is perhaps the most available. Fowler's solution and arseniat- 
ed waters may be used alternately. It must be continued for a long 
time, with proper precautions and intervals of rest, and in full physio- 
logical dosage. Iron may be advantageously combined with it in some 
cases. 

I have not been so successful with nitroglycerin. Gowers praises 
this remedy highly. It is to be given for long, continuous periods in 
doses of 1-200 to 1- 1 50 of a grain three times a day, after meals. Dur- 
ing the paroxysms it should be stopped. It is in the angiospastic type 
of the disease that it exerts its happiest effects, accomplishing it, as 
Gowers says, by regularly flushing the brain with new blood and so 
increasing its general nutrition. 

The continuous use of the bromides has helped some cases, but 
as a rule they are not satisfactory remedies. 

In spite of all we can do in most cases the headaches persist in 
returning. In such instances all we can attempt to do is to mitigate 
the patient's sufferings when the attack is on, or is about to begin. 

Many patients have become so discouraged at the futility of all 
medication that they refuse to be treated, seek a dark, quiet room, and 
await patiently the cessation of the paroxysm. Nitrite of amyl inhala- 
tions may be tried in the beginning of an attack. A cup of strong coffee 
or twenty drops of chloroform has checked it somewhat. Herter rec- 
ommends that the stomach be washed out with water at 105 degrees F., 
and a brisk saline cathartic be administered. The patient should keep 
a recumbent position in bed and a firm hot or cold compress applied 
to the head, and his feet placed in hot mustard water. Menthol may be 
rubbed over the temporal or frontal regions ; instillations of cocaine 
may be made into the conjunctival sac ; and a mustard poultice applied 
to the back of the neck. Electricity does no good and morphine must 
be withheld as long as possible. 

The drugs that are employed to combat the headache are numer- 
ous. In their effects they are very variable. What may be most suc- 
cessful in one case, or in one paroxysm, may fail utterly in another. 
Hence it is wise to have in hand a number of agents to experiment 
with. In most cases a thirty or forty grain dose of potassium bromide, 
sometimes with tincture of cannabis indica or tincture of hyoscyamus, 
repeated every two or three hours, gives considerable relief. Chloral 
produces sleep, but after this wears off the pain comes hack in all its 
pristine severity. Even morphine sometimes acts this way. The coal- 
tar preparations, antipyrine, acetanilid and phenacetine. enjoy an un- 
deserved popularity. In large doses they are apt t<> be dangerously 
depressing, and in small doses they are not rapidly effective. In mild 



234 THE NEURONIC DISEASES 

cases, however, I have gotten some results from all three, administered 
in small, frequently repeated doses. Personally I prefer phenacetine, 
giving twenty or thirty grains, in five-grain doses, every quarter or 
half hour. While taking this remedy the patient should lie down and 
take some brandy or aromatic spirits of ammonia. A few grains of 
caffeine with potassium bromide makes an excellent combination for 
some cases. Sodium salicylate in thirty or forty grains, administered in 
a cup of strong coffee, sometimes suppresses pain. Caffeine may be 
combined judiciously with it. Guarana (paullinia sorbilis) is similar 
to and not much better than caffeine. It may be given in twenty or 
thirty grain doses, repeated every half hour for three or four times. 
The dosage of the alkaloid, guaranine, is one to five grains. 

Other medicaments worthy of a trial sometimes, and always use- 
ful as a reserve force when the others fail, are analgen (5-15 grains), 
exalgen (4 grains), methylene blue {V/2 grains), cytisin (1-20 grain), 
migranin (16 grains), cannabis indica, nux vomica, ergot, ammonium 
chloride, neurodin (15-25 grains), quinine valerianate, thermodin (15- 
20 grains), triphenin (15-20 grains), valerian, aconite and belladonna. 

The drug treatment of migraine is far from being all that could 
be desired. If cannabis indica in full dosage, the bromides with 
hyoscyamus, sodium salicylate, the coal-tar preparations and caffeine 
fail, there is not much to be hoped for from anything else. Hence it 
is best to persist, even in the face of possible ultimate failure, with 
these than to rapidly change from one drug to another of this long list 
of uncertain and often inert preparations. 

As a last resort hypodermics of morphine may be turned to, though 
occasionally even these fail, and in doing so may save the patient from 
the greater danger of the drug habit. 

The seton has seemed almost to have produced a cure in a few cases. 
It is inserted in the back of the neck, the tape is changed fortnightly 
and the wound is dressed daily with one boric fomentation. Watson, 
Cornish and others commend the treatment in obstinate cases. It prob- 
ably acts by counterirritation. 

HEADACHE. 
CEPHALALGIA. CEPHAL^A. 

Headache is only a symptom accompanying many diseased states 
and the term ought to be regarded in the same way that paralysis and 
apoplexy are. As it is so prominent and frequent a symptom, as it is 
so often the only symptom of which the patient complains, and as its 
cause in a certain percentage of cases is quite hidden, it rises almost 
to the dignity of being a special disease, and so perhaps in a work on 
nervous troubles deserves a special section. In a book covering the 
entire field of medicine there would be no need of a special discussion 
of headache, for anything like complete consideration of it would 
include a discussion of the whole field of medicine. 

Not every pain about the head is included under the specific term 
headache. By it is meant a more or less diffuse soreness and pain in 
and about the vault of the head. Facial pains and pains following the 



THE NEURONIC DISEASES 2^ 

course and distribution of particular nerves are regarded as neuralgic. 
The laity sometimes use the term "neuralgia'' when referring to head- 
ache, but for the sake of clearness the above distinction between the 
terms should, for the present, be insisted upon by the profession. 

Headaches are pains of variable intensity, extent and duration that 
occur in the frontal, occipital, temporal and vertex regions of the 
cranium. 

Various classifications have been made upon the basis of location, 
cause, character and relationship to other diseases. All of these classi- 
fications are of some practical value ; none of them are complete or 
entirely satisfactory. The best are undoubtedly those in which the 
causes of the headache, considered on broad lines, are made the 
foundation. 

Etiology. — As I have said, a discussion of the causation of head- 
ache would cover the whole field of medicine. There are certain 
prominent factors, however, that may be profitably dwelt upon. 
Neurotics and people in a condition of nervous depression furnish the 
larger number of victims ; hence heredity, in the form of neuropathic 
transmission, plays a role. Age, occupation, environment, habits, dis- 
sipations, mode of life, all enter into the etiology in so far as they 
cause nervous inadequacy. Including migraine in his statistics, Dana 
finds that headache attacks ten to fifteen per cent, of school children, 
over fifty per cent, of women, and about twenty-five per cent, of men. 

The age at which the special varieties of headache make their ap- 
pearance depends upon the underlying cause. Early adult life for 
both sexes seems to be the favorite period of the disease. The com- 
petition and strain of urban life ; the dissipation and self-indulgence of 
wealth ; the mental overexertion in bad hygienic surroundings ; the 
barometric and climatic changes of various seasons and localities, are 
all elements in determining the frequency of headache. 

From the standpoint of etiology the following types of headache 
may be noted : 

I. Hcemic and Vasomotor. The brain being so abundantly sup- 
plied by blood, as the ultimate seat of consciousness and all painful 
sensations, it would naturally be expected to be affected when the 
integrity of the blood or the amount of its supply is any way disturbed. 
Anaemic and congestive headaches are therefore very real and not at 
all uncommon. The former may be associated with chlorosis, sudden 
and severe hemorrhage or the deteriorated condition following a long, 
exhausting disease. Arteriosclerosis may cause a local anaemia with 
nutritive depression, though Oppenheim suggests that the rigid vessels 
may irritate the meninges. Both active and passive hyperaemia will 
raise the intracranial blood pressure and thus provoke a cephalalgia. 
It may be arterial and caused by sudden emotional excitement, toxicity 
of the blood from alcohol, tobacco, coffee and traumatism; or, on the 
other hand, it may be venous and associated with cardiac, renal and 
pulmonary disease. Faulty position and tight constriction of the neck- 
may impede the circulation. The nutritive value of the blood ma) be 
greatly diminished by the presence of infectious material. Thus under 
the class of haemic headaches we must enumerate all those thai are 



236 THE NEURONIC DISEASES 

associated with such diathetic conditions as gout, rheumatism, diabetes,. 
uraemia; such infectious fevers as malaria, influenza, typhoid; and 
such forms of autointoxication as have their origin in gastric dis- 
orders, constipation, hepatic and renal insufficiency, etc. Thus mechan- 
ically, nutritively and physiochemically are these haemic and vasomotor 
headaches produced. 

2. Toxic. In a smaller number of cases certain poisons probably 
act as direct irritants upon the pain mechanism, causing minute func- 
tional disturbances in the nervous elements that, if continued long- 
enough, may go on to actual neurotic degeneration. In these intoxica- 
tions the effect of the poisons on the histological elements is probably 
partly direct and primary and partly indirect and secondary by way of 
the vasomotor disturbance which they set up. An alcoholic headache, 
for instance, may be both a purely toxic and a secondary haemic head- 
ache. 

Among the numerous toxic agents which we regard as of etio- 
logical importance may be noted alcohol, tobacco, coffee, lead, mor- 
phine, chloroform, ether and others. Foul air in badly heated rooms or 
from defective plumbing, impure water and tainted food may be dan- 
gerous on account of their toxicity as well as by reason of depriving the 
organism of its normal needs. 

3. Reflex. The reflex causes of headache are numerous and 
have furnished the ground for many a sharp battle of opinion. It is- 
perfectly reasonable that peripheral abnormalities should at times pro- 
voke central disturbances, but it is absolutely illogical to affirm that 
all central disturbances are due to such peripheral conditions. 

Through its outstretching processes, the seat of consciousness is 
in close relationship with every tissue and organ of the body. It may 
well happen, therefore, that disease of any one of these outlying struc- 
tures may be such as to set up a high degree of distress in the pain- 
centers of the brain. To enumerate the sources of reflex irritation, one 
would have to give a complete resume of anatomy, physiology and 
pathology. Suffice it to say that they are most commonly found in 
connection with the eyes, the stomach, the sexual organs, the nose and. 
the ear. Errors of refraction and accommodation ; naso-pharyngeal 
hypertrophies, tumors and inflammations; sexual excesses, masturba- 
tion, uterine diseases and menstrual disorders ; indigestion, gastric 
catarrh, intestinal parasites, etc., are among the more common periph- 
eral reflex causes of cephalalgia. 

4. Neuropathic. Under this head we place those headaches that 
accompany epilepsy, neurasthenia, hysteria, neuritis, neuralgia, chorea, 
etc. These partake of the etiology of the disease with which they are 
associated. In my opinion most of them are toxic or autotoxic in 
origin, and not a direct expression of the neuropathy in the way that 
the general neurosis is. For example, neurasthenia is a general neu- 
rotic deterioration; the headache that accompanies it is usually the 
result of the auto-intoxication that develops from the functional in- 
efficiency of the organs of assimilation and excretion. The pain of 
hysteria is usually the result of a psychic or physical abnormal reflex 
influence. And so on for most of these so-called neuropathic head- 



THE NEURONIC DISEASES 237 

aches. Hemicrania, though discussed by itself in another section, 
falls into this class, being- related to epilepsy. 

5. Organic. By organic headaches we mean those that are set 
up by gross, organic lesions easily discovered upon post mortem exam- 
ination, or even during life, and that may or may not be amenable to 
-surgical intervention. Disease of the bones of the skull, meningitis, 
-cerebral syphilis, intracranial neoplasms, arteriosclerotic productions are 
some of these organic causes. Under their respective heads the symp- 
toms will be further considered in detail. 

6. Psychic. Once in a while we meet cases of headache which 
seem to have been brought on by pure psychic influences, and are 
certainly sometimes quickly removed by suggestion and other psychic 
means. Sudden emotion, fright, disappointment, prolonged intellectual 
action, dread, terror and other depressing psychic influences sometimes 
.give rise to headache. In a few cases of masturbation it has seemed 
to me that the headaches and other symptoms were due to the dread 
and shame and fear of insanity, more than to the mere physical stress. 
With Wundt I regard the mental acts as processes and not actual en- 
tities. They are not simple, but complex. They represent the inter- 
play of certain elementary sensory impulses in and among one another. 
If this interplay is suddenly disturbed or shocked it reacts injuriously 
upon the underlying sensory elements and causes them to manifest 
pain. These cases, however, are very rare. 

Pathology and Pathogenesis. — It is somewhat of an anomaly to 
speak of the pathology of a symptom. Only diseases have a patho- 
logical basis, and headache is not a disease. And yet there are some 
facts in regard to the pathogenesis of even a single symptom so promi- 
nent and unique as headache sometimes is that need a moment's con- 
sideration. 

Apart from the pathology of the underlying general abnormality 
upon which the headache depends, there is absolutely no known con- 
stant lesion that can by any stretch of reasoning be distinctly associat- 
ed with the latter. Hsemic, toxic, reflex, neuropathic and organic head- 
aches reveal nothing beyond the usual findings of these respective con- 
ditions which may be singled out as the specific source of the head pain. 
Various theories have been proposed and the cephalalgia has been 
assigned to the implication of the fifth nerve or the nerves of the dura 
mater, the nervi nervorum, the primary and basal ganglia or the 
cerebral cortex. One thing seems to be certain, however, and that is 
that true cephalalgia is not the result of disease in the peripheral nerves 
and their primary ganglia, for this produces the true neuralgias in 
and about the head. The headache pain is too diffuse and otherwise 
unique to be a mere nerve pain. There is nothing beyond mere guess- 
work to assign the pain to the dura mater. Well-known primary and 
secondary diseases of this or the other membranes, aside from the pres 
sure which their thickening may exert upon the cerebrum or related 
nerves, do not provoke true headache. The bead pains of syphilitic 
and tubercular meningitis are pressure pains. To attribute all h< 
aches to the dura mater we would have to assume that in all head- 
aches the dura was diseased and more or less thickened. This would 



238 THE NEURONIC DISEASES 

be an unwarrantable assumption, especially in the total absence of all 
other indications of meningeal disease. 

- The localization of the original source of the pain in the basal 
ganglia, especially the optic thalamus, was strongly argued by many 
at one time. Our more recent knowledge of the physiological functions 
of the basal ganglia is not favorable to this view and it never was 
anything more than a gratuitous hypothesis without experimental or 
pathological proof. 

The only view that has a shadow of a positive foundation whereon 
to rest is that which attributes the pain directly to the functional or 
organic disturbance of the sensory elements of the cortex. Migraine, 
of course, is something more than a mere headache. It is a disease of 
the sensory cortex closely related to that other primarily sensory dis- 
ease — epilepsy. It has many symptoms, but its leading symptom, the 
headache, is in all essential respects the same as the various types of 
headache now under discussion. Therefore if migraine is a cerebral 
sensory phenomenon, why not the cephalalgias that so closely imitate 
its dominant symptom, the headache? In their immediate causation 
the same toxic, reflex and other factors play a significant role. In 
their diffusiveness, changeability and localization they are not unlike. 
Even in some of their manifestations other than the mere pain they 
bear a remote resemblance. And in their management the same gen- 
eral specific medication obtains. In other words, let the cause of the 
trouble be what it will, as well as the general nature of the disease or 
its collateral symptoms, the headache, every indication shows, is a 
functional disturbance of the sensory cerebral cortex. 

It is quite impossible to account for the location of certain head- 
aches in particular parts of the head. Psychic auto-suggestion may 
have something to do with it, as, for instance, the localization of the 
ocular reflex headaches just above the eyes. 

The location of the irritative lesion, as in some of the organic 
cases, may determine the location of the headache. In most of the 
cases there is no sort of imaginable way by which the concentration of 
the pain upon this or that side of the head, in front or on top, can be 
accounted for. This very indefiniteness is an argument in favor of its 
cerebral origin, it seems to me, for in this respect at least it resembles 
the psychoses, which are positively accepted as of cortical origin, but 
without a more definite seat within the cortex. Like the latter it is a 
functional trouble of the sensory cortex more or less in toto, rather 
than of special centers of sensation in that cortex. 

Symptoms. — Cephalalgia is a diffuse, changeable soreness or pain 
of the head or various parts of the head. It may be superficial and 
aggravated by slight percussion. Steady pressure often relieves it. 
Sometimes it is dee]), concentrated and boring. At other times it 
resembles a paresthesia and is described as burning, cutting, pressing. 
pulling, sticking like pins and needles. Usually the seal]) is hyper- 
aesthetic. 

The character of the pain and its action under different conditions 
are sometimes dependent upon the immediate cause of it. The same 
may be said of its location. For instance, anaemic headaches are dull 



THE NEURONIC DISEASES 



239 



and heavy, are not particularly severe and are spread more or less 
over the entire scalp, the brow or sides of the head. The recumbent 
position usually alleviates them. On the other hand, the congestive 
headaches are full and throbbing, combined with vertigo and aural 
disturbances, visual phenomena and redness of the face and con- 
junctivae. The recumbent position aggravates these. 

The location of the headache is often strongly suggestive of its 
cause, though no absolute rules can here be laid down. The larger 
number of the head pains are frontal ; next in frequency are the oc- 
cipital headaches. Vertical and lateral localization of the pain is not 
uncommon and often generalized combinations of these are met with. 
Pains that are more or less constant and are localized in the supra- 
orbital region are apt to be due to ocular defects or dyspepsia. If the 
pain here is absent in the morning and appears in the afternoon it is 
due to eye-strain. In neurasthenia I have often noticed that the patient 
will get up with a slight frontal soreness, which will disappear for a 
few hours, only to return later on in still greater severity. Auto- 
intoxication headaches, with constipation, are dull and constant over 
the upper part of the brow. Sharp, boring, burning pain on the vertex 
is a neuropathic headache. As clavus it is typical of hysteria ; as a 
full, compressing or lead-cap feeling it is probably neurasthenic. A 
steady, duller ache on the top of the head should cause us to look for 
anaemia, uterine disease, possibly stomach or bladder trouble. Occipital 
soreness is mostly uterine or gastric in origin and is often accompanied 
by nausea. There may be vertigo. Temporal headaches, particularly 
if they are unilateral, keen and persistent, are neuralgic or migrainous. 

In the diagnosis of the headaches of organic origin, say from 
tumor, exostosis or meningitis, one would not rely alone on the pain 
symptom. In every case a most thorough search ought always to be 
made for collateral symptoms. These will often interpret most con- 
clusively the cause and nature of the head pain. 

The persistency of the headache will suggest a persistent cause, 
like caries of the teeth, tumor; headaches that come and go may be 
merely neurotic or indicate their dependence upon conditions that are 
subject to changes, such as nerve tire, constipation, gastric activity and 
quietude. 

Diagnosis. — The mere diagnosis of headache is no diagnosis at 
all. The underlying cause or disease that provokes the pain is tin- 
ultimate purpose of the examination. It is always a confession of 
defeat, unfortunately sometimes unavoidable, to write a prescription 
with no better end in view than merely to suppress the pain. Head- 
ache is like the wreath of smoke that should lead at once to the threat- 
ening fire. The latter is not extinguished by blowing away the smoke. 
Hence of all the symptoms met with in the practice of' medicine none 
needs a more careful study. I am convinced that in making a diagnosis 
in headache the errors will be less in number just in proportion as the 
examiner keeps his mind off of the headache itself and turns his 
scrutiny upon the collateral symptoms of the possible disease that is 
causing the headache. In other words, let him minimize as much 
he can the cephalalgia in the drawing up of the clinical 'picture of the 



24-0 THE NEURONIC DISEASES 

case in hand, and emphasize all the other symptoms that may be pres- 
ent. For instance, search keenly for the symptoms of neurasthenia, if 
there is an intimation that the head pain is neurasthenic in origin ; 
rather dwell upon the paresthetic, lead-cap character or what-not of 
the headache. Delay not with the dull, aching, diffuse character of a 
possible anaemic headache, but make a blood examination and deter- 
mine the presence of anaemia. Be not satisfied with a supra-orbital 
headache as of ocular origin, but study the case as though it had pre- 
sented itself primarily as one of eye trouble. 

In the books and in practice too much reliance is put upon the 
location and character of the headache as indications of its cause. They 
can only offer the barest sort of hints. 

So variable are the different types of headache that one may some- 
times easily be mistaken for another. Authors lead their readers into 
a feeling of treacherous self-security by telling them that each sort of 
headache has its own marked and distinctive characteristics. The 
characteristics are quite shadowy and scarcely ever more than barely 
suggestive. Exceptions are all" too frequent to the general rules laid 
down in the books. The only safe way to do is to search for and 
diagnose the primary disease on top of which lurks the headache that 
induced the patient to consult the physician. 

Prognosis. — This depends so absolutely upon the underlying 
cause that nothing further need here be said about it. 

Treatment. — The proper treatment of headache is the removal 
and treatment of the underlying cause. Anything short of that is a' 
mere makeshift. The shops are full of so-called headache remedies, 
sure-cures and patent nostrums. A physician who> treats a case of 
headache that presents itself at his office by prescribing a pain-killer 
or -shot-gun sedative mixture, without attempting to find out and re- 
move the cause, is exercising about as much intellectual acumen as 
the individual himself would do if he had first gone to the drug store 
and asked for one of the much-lauded headache cures. The laity rec- 
ognize this and reason to themselves justly and unanswerably that 
there is nothing gained, but something saved, by not consulting such a 
physician. Much of the rampant quackery and counter-prescribing of 
the day is thus fostered, and such physicians can take much of the 
blame for it to themselves. 

Every case of headache indicates some disease of more or less 
severity, and though a physician may at first attempt to give the pa- 
tient comfort by annulling the pain, his duty and his reputation both 
demand that he insist upon the patient joining him in regarding his 
trouble as something more than mere head pain, and in allowing him 
to search for and remedy so far as possible the disease of which the 
headache is one symptom. Under the head of etiology I have pointed 
out some of the more prominent of these troubles, and their treatment 
must be sought for elsewhere. I will mention here merely some of 
the means of relief to be employed temporarily. 

If the headache is at all severe it is well to minimize as much as 
possible all sources of peripheral, sensory irritation. The patient 
should occupy a dimly lighted, still room, comfortably warm and with 



THE NEURONIC DISEASES 24I 

free ventilation. The clothing must be loosened and, better still, re- 
moved entirely in some cases. The cutaneous sensation should be kept 
as quiet as the visual and auditory. A warm bath is sedative in this 
respect. If there is congestion of the head, mustard pediluvia are 
useful, but they must be employed for half an hour at least. Except 
in a few instances of occipital headache mustard to the nape of the 
neck is irritating and not equally compensating. In extreme cases 
two or three leeches behind the ears may have to be resorted to. Dry 
cups to the shoulders and upper spine have helped some of my cases. 
The effect was partly psychic, I am sure. Electricity is useless. Gentle 
rubbing and stroking of the head, the cold water coil, the ice bags or 
hot cloths to the brow and nucha may be tried. Rubbing the temples 
with the menthol stick or a twenty per cent, solution of menthol, or a 
chloroform liniment is sometimes useful. Only alleviation, however, 
can be hoped for from all such external applications. The stinging of 
the skin diverts the attention temporarily from the cephalalgia. In 
most cases much more can be anticipated from a brisk cathartic given 
early. Calomel, salines, jalap powder, elaterium and croton oil are 
available for this purpose. 

There are many remedies that may be given, but their effects will 
vary in different cases. Phenacetine has been the most generally useful 
in my experience. A ten or fifteen grain dose is given at once, and five 
grains every hour or half hour thereafter until about fifteen grains more 
are taken. Then I continue the remedy in five-grain doses every two, 
three or four hours. It is well sometimes to give a little brandy or 
aromatic spirits of ammonia at the same time, and to insist upon the 
patient retaining the recumbent position. Antifebrin and antipyrine may 
be used instead, though in my experience they have threatened collapse 
several times. An excellent pain sedative sometimes is a thirty or forty 
grain dose of sodium salicylate. Muriate o>f ammonia in doses of a 
dram or half a dram is recommended. Some of the remedies sug- 
gested under the head of hemicrania may be tried. Such medicines as 
aconite, cannabis indica, nitromuriatic acid, digitalis, belladonna, col- 
chicum, ignatia, nitroglycerin, sodium bicarbonate and valerian should 
be thought of when the particular conditions present call for them. 
Caffeine alone, or with full doses of the bromides, is available. Hydro - 
bromic acid, aromatic spirits of ammonia and valerian have assists 1 
me in some cases. Butyl-chloral hydrate, camphor, chloralamid, ethy- 
lene bromide, gelsemium, guarana, hyoscyamus, kola and quinine con- 
stitute an experimental list which it may be convenient to have ready 
at hand when the case is obstinate. As a last resort the stronger nar- 
cotics may be used. Even morphine fails sometimes and there is 
always the danger of establishing the habit in these cases. 

So desperate are the cases sometimes that even blood-letting and 
the introduction of a seton have found approval. 

In no trouble is the physician's skill and resources put to a more 
severe test. The greater these are the happier he will he. I le should 
never allow himself to be so resourceful, however, as to thereby be 
rendered forgetful of the fact that the fundamental treatment of head- 
ache is first, last and all the time the steady and persistent treatment 



2^2 THE NEURONIC DISEASES 

of the underlying- disease or defect out of which the cephalalgia is but 
a mere by-product. 

THE NEURALGIAS. 

The term neuralgia means literally nerve pain. In a broad sense 
every pain that is experienced is a neuralgia. In this way the laity 
still speak of headache sometimes as a neuralgia. In neurology we 
have restricted the use of the term to pains that can be definitely local- 
ized in the nerves of the body. Indefinite and diffuse pains and mere 
psychic distress we do not include in neuralgia. 

The explanation and definition of pain has been the problem of 
the ages, and we are almost as far from its solution as ever. Pain 
is a phenomenon, a manifestation merely. It is not a thing itself, but 
merely represents the activity of some thing. Just what this thing 
is, and at what point this form of its activity ceases to be normal and 
becomes abnormal, is the still unanswered riddle. The localization of 
the phenomenon we call pain and the determination of its relationship 
to what we are pleased to denominate normality would, if known, 
dispel a vast amount of confusion and contradiction in regard to all 
neuralgia. 

I will endeavor in as few words as possible to make clear the 
position of modern neurology in regard to these two important ques- 
tions, and I think it will help us to classify and comprehend better 
the specific forms of neuralgia now about to be considered. 

It is conceded by every one that the experience of pain is dependent 
upon the nervous elements. If the nervous elements of the body could 
be in some miraculous way dissolved out of it, without in the least 
disturbing the bones, muscles and other tissues, there would absolutely 
cease to be all pain or possibility of pain. 

In what part of the nervous system does this function of the pain 
sense reside? Both experimental and pathological observations prove 
that the neurones, the true nervous elements, the cell-bodies with their 
processes, constitute its seat. The neuroglia, the connective-tissue and 
the blood-vessels, the sustentacular elements interwoven with the net- 
work of neurones, do not subserve in any way the awakening or the 
transmission of the pain sense. By the aid of certain experimental 
and pathogenetic degenerative processes we have learned pretty ac- 
curately just which sets of neurones it is that are sensory. There are 
so many different forms of sensation, such as touch, temperature, pain 
and special sense, and the neurones that subserve them are all so closely 
intermingled, that only in connection with one or two of the special 
senses are we able to say just what sets of neurones belong to each 
respective form of sensation. We can pick out, as it were, the visual or 
the auditory neurones, but we cannot pick out the pain-sense, the tactile 
and the temperature-sense neurones. We can only speak, then, of 
general sensory neurones and special sensory neurones, and in a gross 
way we can point out where each respective set is to be found. 

When we examine, by staining and microscopic methods, these 
sensory neurones and compare them with what we have learned to be 
the motor neurones, we discover that apparently there is no essential 



THE NEURONIC DISEASES 243 

difference in their intimate structure. I say apparently, because even 
yet we dare not assume that our modern means of investigation, mar- 
velous as they are, are absolutely perfect, reliable and ultimate. With 
our present means of investigation, however, we make bold to assert 
that all neurones of the body, sensory, motor and trophic, are, except 
in some obviously and functionally unimportant particulars, structurally 
alike. This assumption is strengthened in part, as I have pointed out 
elsewhere, by the fact that the manifestations of nervous activity 
are revealed to us not in the nervous elements themselves, but in their 
related end organs. Motion is not, strictly speaking, a nervous, but a 
muscular phenomenon. Vision, hearing and touch are manifestations 
or experiences evolved by special extra-neural apparatus connected in- 
timately w T ith similarly constructed nervous elements. 

As on the motor side, so on the sensory, then, we assume that the 
neurones are not only structurally the same, but functionally the same, 
and that their apparent differences of function are dependent upon the 
particular end organs with which they happen to be connected. 

Though the proofs from the laboratory are not yet absolutely be- 
yond question, they are so strongly in favor of the uniformity of 
nervous matter everywhere, both in structure and function, that it has 
almost become an axiom in neurology that there is a specific nerve- 
energy, a form of irritability merely, which is the same everywhere, 
but which is revealed in various ways through the various non-neural 
tissues and organs with which the nerve elements are in organic, 
functional relationship. If this is so, then we must look to the ends 
of the pain-sense neurones for the explanation of the nature of pain. 
Unless we add pain as an additional form of energy in the nervous 
elements to the one universal specific nerve-energy, irritability, we 
must account for the pain, just as we do for motion, for secretion, for 
vision, for hearing, for taste, for touch and so forth, by the presence 
of some extra-neural mechanism. If it be so added as merely another 
form of neurility, it would have to be a characteristic of motor neu- 
rones too. 

Analogical reasoning bears us out, therefore, in the contention 
that pain as a specific sense is the result of nervous irritability working 
in conjunction with some sort of extra-neural structure or mechanism. 

There are many gross observations in physiology and clinical prac- 
tice that lend color to this conception of the nature of pain. I will 
now refer to these somewhat in detail, as they will have to do with the 
relationship of pain to what we are pleased to call normality, and 
which I said was the second great problem to be solved in connection 
with this very commonplace phenomenon called pain. 

Having shewn that the trend of modern neurology is toward af- 
firming positively that pain is not a neural manifestation per se, but the 
expression of mere neural irritability, responding to the abnormal work- 
ing of some extra-neural tissue or mechanism, it behooves us to point 
out as far as possible where and what that extra-neural mechanism is. 

It will be conceded that sensory, like motor neuronic irritability. 
needs for its manifestation an external stimulus. It will doubtless be 
also conceded that for its proper termination into what we call pain, 



244 THE NEURONIC DISEASES 

and not into some other form of sensation, the irritability must expend 
itself upon some specific organ or mechanism. 

The stimulus is from without and is in the form of an irritation. 
If the stimulus can originate in the neurone itself and provoke thus the 
specific sense of pain by expending itself solely within the neurone, 
apart from its central connections, we would be forced to go back 
again and believe that the evolution of pain is a specific form of nerve- 
energy. 

A stimulus may come from a degeneration or other nutritional 
molecular change in the neurone, or in a part of it, say at the outer end 
of its peripheral process, but the stimulus will have to pass out of the 
neurone in some way to provoke pain unless we believe that the pro- 
duction of pain is a function of the neurone, which would, of course, 
destroy the axiom that there is only one specific form of nerve-energy, 
mere irritability. 

Stimuli we find may be conceived of as extra-neuronic and intra- 
neuronic. The extra-neurcnic forms of stimulation, both in health 
and in disease, are of common observation and form the source of nine- 
tenths of our pain sensations. The intra-neuronic forms of stimula- 
tion are probably best evidenced in the peripheral degenerative troubles 
in the sensory nerves. These are not common, though they may be 
assumed to be the basis of some of the pains of certain general and 
localized, mild or severe, degenerative troubles, like pseudo-tabes of 
the Dejerine type, of a few cases of so-called peripheral degenerative 
neuritis from alcohol, arsenic, etc., and possibly from some forms of 
neurosis like neurasthenia. 

These peripheral degenerations are not uncommon, but it is always 
a question whether they are primarily degeneration and not secondarily 
degeneration from a compressing inflammation, new growth or other 
lesion in their close proximity. Granting that we do have an inherent 
peripheral stimulus in this occasional primary peripheral degeneration 
in the neurone that subserves normally the pain-sense, we have an ex- 
planation of the specific primary degenerative neuralg'ias referred to 
in the books. 

This stimulus must expend itself centrally upon some special cell, 
organ or mechanism to produce the specific sense which we call pain. 
We find the cell bodies of the sensory neurones scattered all the way 
up and down the nervous tracts. This I have pointed out in the earlier 
chapter on the neurone and the neuronic architecture of the nervous 
system. 

Are the central sensory cells individually the pain-sense centers? 
We find sensory cells in the posterior root ganglia, in the posterior 
oornua, in the bulbar ganglia, in the central ganglia of the brain and 
in the cerebral cortex. Which of them subserve the pain-sense; and 
were we able to determine which, would the cells themselves be the 
mechanism wherein the incoming sensory impulse is transformed into 
a pain-sense" It would hardly seem so, for if a sensory nerve he cut 
oft from its cutaneous connections and the proximal end of it be irritat- 
ed, pain is experienced. If under such circumstances the transforma- 
tion of this afferent impulse into the specific pain sense be accom- 



THE NEURONIC DISEASES 245 

plished by the individual cell to which the impulse has centrally arrived, 
apart from this cell's connection with all other cells, we will again be 
driven to attributing to these cells both a specific structure and func- 
tion. We will then have to relinquish the idea again that nervous ele- 
ments have all only one and the same function, the manifestation of 
irritability, and that their differences of function depend merely upon 
their connections. This will not be necessary, however, it seems to me, 
for there are many clinical observations that go to show most sus- 
piciously that the sensory cells are not individually the centers for the 
transformation of mere afferent impulses into specific pain sensations. 
Chief among these observations are the following : 

1. The obliteration of consciousness by ether narcosis abolishes 
all pain sense, without, so far as we can see, abolishing the functions 
of the afferent neurones generally. Of course, all sensation is largely 
subjective and the patient's ego being for the time in abeyance, there 
are no subjective results from peripheral stimulation. Some of the 
reflexes that are outside of the sphere of consciousness are still active ; 
for example, the visceral reflexes. Here the sensory cells are apparently 
still intact and so far as we know they are not essentially different from 
the cells that functionate in the conscious sphere. 

2. In the same line of proof is the fact that memory retains spe- 
cific forms of sensation, when the usual sources of the afferent im- 
pulses are removed, as is seen in cases of amputation. There may be 
some question as to whether consciousness is co-extensive with the 
entire nervous apparatus or is to be confined solely to the brain. In 
regard to memory there is no such question, however. Memory is a 
brain function, or at least not a spinal cord function. Most de- 
structive diseases of the cord can occur without the slightest weaken- 
ing of the memory. In the amputations, therefore, in which memory 
retains sensory pictures, it would be demonstrated that the functions 
of the cord cells and brain cells are different. Cord cells don't memor- 
ize, consciously at least; cortical cells do. As the cells are the same 
functionally and histologically, though, we must search for another 
reason for the difference in their functions in this respect. It is to be 
found outside of the cells — namely, in their relationship and interplay 
with other cells. It is in the mind. 

In its last analysis, then, pain is a pure mental manifestation, h is 
not a specific form of nerve-energy. It is not a direct product of 
individual cellular activity. It is dependent upon the activity of certain 
cells for its expression. It is a psychic phenomenon, with all the 
variability and all the uncertainty that goes with a complex manifesta- 
tion of a complicated physical interplay of individual physiological 
units, such as the mind is. 

Pain is not an entity. It is a psychic experience ; one of what 
Wundt well calls the psychical elements. Being dependent for its pri- 
mary evolution upon the activity of a physical basis, it assumes a phys- 
ical appearance and we speak in common parlance of physical pain. 
On the other hand, being a psychical element and partaking of all the 
characteristics of mind, we speak of it as a psychical pain. 

There can obviously nor be two kinds of pain that are identical 



246 THE NEURONIC DISEASES 

and yet different at the same time. The difference between physical 
and psychical pain is one merely of the nature of the stimulus and the 
underlying physical basis. Like the distinction between colors, which is 
a purely psychic or cerebro-psychic phenomenon, and which we project 
into the outer world by attributing the colors to the objects or sources 
of the visual stimulation, so the pain, which is a psychic experience, 
is projected outward and we say that the pain is in that nerve or this 
organ, whereas the latter is only the objective source of the stimula- 
tion. 

This has all a most practical bearing and if the general truth un- 
derlying it is fully grasped, it will not be difficult to realize that a 
psychic pain, such as may occur in hysteria and other psychoneuroses, 
is as much of a reality as is a pain caused by a corn on the toe. In 
neither case is the pain sense per se different ; in either case it is a 
psychosis due to different sources of stimulation. In the latter case 
we can reach the source of stimulation with the knife and salves ; in 
the former case there is a disturbance in the functional interplay of the 
psychical elements of such a nature that neither surgery nor medicine 
can reach, but only psychic measures which belong to the same sphere 
of action, the psycho-neurotic, that the disease does. 

Extra-neural stimuli of so-called physical pains are as a rule very 
amenable to treatment, and their prognosis is generally favorable. In- 
tra-neural (neuronic) stimuli which produce both the so-called physical 
and mental pains, are very obstinate to treatment and possess a rela- 
tively hopeless prognosis. 

As the pains of the first sort were the most obvious and the first to 
be recognized boldly, and as the particular nerves involved in the extra- 
neural lesion were clearly and easily discoverable, nerve pains came to 
be identified with individual nerves and the term Neuralgia acquired a 
very narrow meaning. So fixed is this meaning now that it would be 
hazardous in the extreme to use it in any broader sense. I will there- 
fore continue to employ the term as a synonym for a pain that can be 
referred to some particular nerve or nerves. As these nerves are sub- 
ject to inflammation, compression and destruction, they will be appro- 
priately discussed under their own individual heads in the section 
devoted to the non-neuronic affections in the latter part of this book. 
I [ere, however, ought to be noticed those neuralgias which are, or may 
be, referred to particular nerve trunks, but which reveal no discoverable 
changes in or out of the constituent sensory neurones, which are of 
central origin and which therefore partake of all the traits of a true 
psychoneurosis. 

These are what some writers mean by the primary or essential 
neuralgias. Like all similar neuroses they have a neuropathic heredity 
behind most of them, or occur as a part of a general neuropathic state; 
are probably the expression of a congenital, nutritive deterioration of 
greater or less degree in the general neuronic elements of the nervous 
system; are of doubtful, often hopeless, prognosis; and are not very 
amenable to treatment except through general tonics, powerful seda- 
tive^, isolation, disciplinary and psychic measures, by which they may 
sometimes be considerably helped, but not cured. 



THE NEURONIC DISEASES 247 

Clinically it is not always possible to differentiate an idiopathic 
neuralgia from the pain caused by neuritis, reflex irritation or neigh- 
boring disease. This is because both may be of such a slight degree 
that the characteristic symptoms of either are not well marked. The 
difficulties of practice should not, however, be allowed to interfere if 
possible with the accurate presentation of the known facts of science. 
A neuralgia that is a mere reflex pain does not seem to me to be prop- 
erly classified as a disease, though it is proper to refer to it in a work 
upon nervous disturbances, just as we there also refer to other normal 
functions of the nervous system. A neuralgia, for instance, that is 
caused by a cicatrix, a bad tooth or loose internal organ, I would call 
attention to, not as a nervous disease, but as a disease overworking a 
normal nervous function. It is to be corrected by removing the cause, 
but it is certainly not a "true idiopathic" neuralgia in the sense of 
being a disease any more than the sudden touching of a hot plate or 
the prick of, a pin is a neuralgia in the sense of being a disease. 

This is an important distinction, for practically all of the so-called 
reflex neuralgias are of this character and need no treatment other than 
removal of the source of the reflex. Every nerve pain should be ex- 
haustively examined for a possible irritant of this sort. 

This leaves then only the inflamed nerves to be differentiated from 
the idiopathic pains. 

A careful consideration of the pathological condition in neuritis, 
and the absence of such a condition in primary neuralgia, will help 
one to realize the difference in the clinical presentation of the two 
troubles. The former is locally irritant and compressing ; the disease 
process is not uniform throughout the entire nerve length ; the nearby 
motor elements are implicated in the damage, along with the sensory ; 
and there is a rather sharp limitation of all the sensory and motor 
signs to the one nerve and its area of distribution. 

Idiopathic neuralgia, on the other hand, is a central neurosis, there- 
fore there are no marked locaf manifestations ; the nerve is sore, to 
be sure, but it is not sharply and distinctly locally sore ; the whole 
nerve is equally sore. The pain is a referred pain. I recently saw a 
case in consultation that had been vigorously treated locally with mas- 
sage, electricity, etc., as an instance of sciatica. The pains were 
paroxysmal and complained of almost entirely in the foot and a short 
way up the leg. Pressure on the nerve caused soreness, but not pain. 
I diagnosed intrapelvic secondary irritation, which proved to be abun- 
dantly present upon further examination by a surgeon of ability. 

Idiopathic neuralgia has no motor symptoms except what may 
be caused in a general way by the pain of movement. There are no 
electrical reactions. No atrophy appears except late in the disease. 
The paroxysmal character of the pain indicates its idiopathic nature, 
though it must be remembered that a mobile source of irritation to the 
nerve may cause a mere reflex pain to come and go like a paroxysmal 
trouble. A tender nerve can, of course, be made still more painful by 
sudden movements, jars, coughing and sneezing. I have found stretch- 
ing of a nerve that caused marked exacerbation of pain, say by forcible 



248 THE NEURONIC DISEASES 

flexion of a limb, to be rather indicative of a neuritis than an essential 
neuralgia. 

Early motor, other sensory symptoms with the pain, and trophic 
manifestations point to neuritis. In fact, pain and only pain constitutes 
the entire clinical picture of neuralgia. 

Late trophic symptoms of a general character, like falling of the 
hair, etc., may be due to the same general neuropathic condition of 
which the neuralgia is itself one evidence. 

Changeability of neuralgia is in marked contrast with the fixity 
of the neuritis. It is not an uncommon thing for a primary neuralgia 
to suddenly transfer itself to the corresponding nerve on the opposite 
side of the body, or to some other remote nerve. Hyperesthesia of a 
slight degree, but never anaesthesia, sometimes occurs late in the area 
of the skin innervated by the affected nerve. The pressure points of 
Yalleix are as a rule indicative of neuritis, being the local spots in the 
nerve where the inflammatory spots are most exalted. In neuralgia, 
however, they may indicate where the sore nerve happens to pass over 
a bony edge or prominence. 

Prolongation of the pain has its general depressing effect upon 
the constitution, though it must be remembered that primary neuralgia 
is mostly observed in depressed, cachectic and neuropathic individuals. 
Mild psychosis, such as melancholia, is often present. Suicide is 
thought of in many severe cases. 

The causes of primary neuralgia are the general cachectic, infective 
and toxic states. Mental shock may cause it. Debility is the most 
frequent cause. It is doubtful if malaria is so much a cause as it is 
supposed to be. Neuralgia is not more common in malarious districts 
than elsewhere. One must not confuse the neuralgia of the general 
debilitated state induced by rheumatism, gout, Bright's disease, lead 
intoxication, diabetes or exposure with the neuritis often produced by 
the same causes. 

Women of neuropathic families are the greatest sufferers from the 
disease. Children and the aged do not have to endure it. It is prac- 
tically unknown before fifteen years of age. 

The following are some of the more prominent forms of idiopathic 
neuralgia and their treatment : 

Tic Douloureux. Trigeminal Neuralgia. Prosopalgia. This is 
a frequent form of idiopathic neuralgia. It should always be carefully 
distinguished from symptomatic pains in the fifth nerve, from various 
lesions and sources of irritation around and near it. The latter are very 
common and will be referred to again under the head of special dis- 
eases of the fifth nerve. In tic douloureux the patients are usually 
neuropaths in the middle period of life. 

All branches of the nerve may be the seat of the pain and the 
trouble may be unilateral or bilateral. The paroxysmal and intense 
character of the pain is a marked feature of it. Usually it is limited to 
one branch of the nerve and is most excruciating. It is described as a 
feeling like a boring piece of hot iron, or a hot knife cutting into the 
Face. All movement is avoided. Tenderness is felt and even twinges 
of pain in neighboring nerves. From the cheek, the lips and side of the 



THE NEURONIC DISEASES 



249 



nose, where the pain is usually at its maximum, it seems to radiate 
into the teeth, over the eye, up or to the head and- across the temple. 
The face becomes red, the eyes water, the flow of saliva and nasal 
mucus increases. The agony lasts a few minutes and then the pain 
partially recedes. It usually returns again and the new paroxysm may, 
like the first, be started by some simple irritation against the skin. 

Long standing cases may be accompanied after years of suffering 
by premature turning gray of the hair and in rare instances facial 
hemiatrophy. 

The disease usually involves the supra-maxillary branch on one 
side. The supra-orbital and inframaxillary branches are less often im- 
plicated. 

Changes of the weather sometimes affect the pains and they are 
worse as a rule in winter than they are in summer. The severe forms 
of these neuralgias that sometimes occur in the aged were called 
epileptiform by Trousseau. 

In the diagnosis of tic douloureux every possible reflex and symp- 
tomatic pain of the nerve should be eliminated. It is to be frankly 
admitted that this cannot always be done. It is to be remembered, 
then, that pure idiopathic neuralgia of the fifth nerve is far less fre- 
quent than any of the other forms. One should always be on the alert 
to recognize at any time symptoms that point to some other cranial 
disease which has caused the pains. If the patient is neuropathic, if 
there is a heredity, direct or indirect, behind the disease, if the pains 
are markedly paroxysmal and severe, almost epileptiform in character, 
and if they constitute the entire ciinical presentation in the case, a 
diagnosis of tic douloureux will probably be correct. 

The treatment of tic douloureux is not a very grateful task. It 
is a most obstinate trouble and often resists all measures. Sometimes it 
ceases all at once. Would that we could always take the credit for this. 

Every case must be managed along general lines and treated for 
the paroxysm. The whole physical and mental being must be built up. 
Change of scene, change of thought and entire change of environment 
may be necessary. The diet must be abundant, plain and nutritious. 
The functions of the body must be systematically attended to. Tonics 
like iron, quinine, cod liver oil and hypophosphites, and especially 
arsenic, may be judiciously administered. All defects, such as circula- 
tory weakness, poor blood, insufficiency of the kidneys, ocular anoma- 
lies, sluggish liver, must receive their quota of attention. In some 
cases general treatment along these lines will cause the paroxysms to 
cease entirely, or, what is more likely, to remain farther apart and be 
less severe. 

The treatment of the paroxysms will indeed tax the physician's 
resources to the uttermost. It is discouraging to read the long list 
of remedies that are recommended, and yet that generally prow Ii 
Still something must be done, and as amelioration does sometimes most 
unexpectedly follow the administration of a remedy, we must go on 
giving them, even though it be like a forlorn hope. In aged persons 
nitroglycerin, gr. 1-100 every three or four hours, has been effective. 
Anaemic cases may have their attacks aborted by an inhalation of 



250 



THE NEURONIC DISEASES 



nitrite of amyl. Sodium salicylate in twenty or thirty grain doses may 
be successful. Quinine, arsenic, gelsemium and potassium iodide in 
full dosage are occasionally available. The last should be given es- 
pecially if there is the slightest history of syphilis in the case. Co- 
caine instillations into the conjunctival sac, and painting of the nasal 
mucous membrane with five or ten per cent, solutions may afford tem- 
porary relief. 

Butyl-chloral, croton chloral, codeine, narceine, napellin, neurodin, 
stramonium, pyramidon, atropine, cannabis indica may be experimented 
with. The coal-tar preparations were useless in my experience. 
Duquesnel's aconitine has been useful in some of my cases. 

The employment of morphine must be instituted with extreme 
caution. Dana recommends for cases not over four or five years' 
standing rest in bed with massive doses of strychnine. I have seen 
this succeed in one case. The drug is given hypodermically in doses 
of gr. 1-30 once daily and gradually increased until gr. 1-6 or 1-5 is 
reached. This is kept up for four days, and then gradually reduced. 
Absolute quiet is enjoined in bed. After a month iron and potas- 
sium iodide are exhibited. The treatment can be repeated with less 
vigor. 

Certain local measures sometimes relieve the pain. I have referred 
to the use of cocaine. Local freezing with a methyl chloride spray, or 
the application of extreme heat, may bring relief temporarily. Schleich's 
subcutaneous local application consists of a solution containing cocaine 
gr. ] l / 2 , morphine gr. y±, sodium chloride gr. iv^2 and water giij. 

Compression of the carotid arteries may be tried. 

Electricity is often beneficial, but it may have to be used in various 
ways. Oppenheim curiously secured temporary good results with a 
powerful faradic brush applied to the soles of the feet. This was 
probably a psychic result. The electricity is usually directed as near 
as possible through the affected nerve, or it may be applied to the 
cranium or to the sympathetic nerve in the neck. Galvanic, faradic, 
static and cataphoric forms may all be employed. Galvanization of the 
Gasserian ganglion is the most generally useful method. 

Electrotherapy so often fails that I am inclined to attribute the 
supposed cures from it to the power psychic effect usually produces on 
these neuropathic individuals. 

Operative procedures often give prolonged temporary relief, but 
after them, just as in spasmodic tics, the trouble comes back. The 
very nature of the trouble, a central neurosis, would lead me to expect 
that sort of a result. However, in some of the frightful cases a tem- 
porary relief of several months amply pays for the risks of the opera- 
tion. Neurectomy, extraction of the nerve and intracranial resection 
of the nerve and the Gasserian ganglion are the procedures resorted to. 
Their description belongs to the works upon surgery. 

Glossodynia doubtless should be classified here. 

Occipital Neuralgia. As a pure non-symptomatic form this is ex- 
ceedingly rare. Usually disease in the upper cervical vertebrae, or their 
neighborhood, and hysteria, are the causes of the pains in the upper cer- 
vical nerves. When the neuralgia is idiopathic, unlike the other forms 



THE NEURONIC DISEASES 25 I 

here, it is unilateral, paroxysmal and intense. Tender points are elicited 
at .the exits of the nerves. The pains may alternate with those of tri- 
geminal neuralgia. The treatment is the same. 

Cervico-brachial Neuralgia. This is very rare idiopathicallv, most 
•cases being due to rheumatism and other obvious causes. In neuras- 
thenics and hysterics pains shoot around the shoulder and down into 
the arm and into the digits, following the course of the nerves, particu- 
larly the ulnar nerve. Most of the cases of cervico-brachial neuralgia 
that I have seen were cases of neuritis. The diagnostician must be on 
his guard in regard to these pains, for often they represent meningeal 
and other organic spinal cord lesions. Their treatment, after eliminat- 
ing all sources of irritation and all organic disease, is the same as for 
all idiopathic neuralgias. 

Intercostal Neuralgia and Mastodynia. This is second in impor- 
tance only to facial tic douloureux. The left side is usually affected and 
mostly in women. Several nerves are affected at the same time, so 
that the pain seems to be in the side of the thorax. Sometimes the 
radiation of the pain extends to the inner side of the corresponding arm. 
So many causes produce pains around the body that one must be most 
keenly on the alert for other diseases and troubles that may be the 
cause of the intercostal pains. Always remove these causes. If the 
pain still continues, then the usual measures recommended for all 
idiopathic neuralgias are to be employed. In mastodynia the neuralgia 
is limited to the nerves that go to the breasts. They are branches of 
the intercostal nerves. The pains are paroxysmal and intense and seem 
to spring from those nerves that come off from the fourth to the sixth 
intercostals. The skin is hypersesthetic and the breast tender. Herpes, 
of course, does not occur in idiopathic neuralgia, only in neuritis. The 
pressure points are here over the second to the sixth spinous processes. 
Women of middle age are usually affected ; men very rarely. Excit- 
ing causes may be pregnancy, lactation, fissures, trauma and mental 
excitement. It is a stubborn neuralgia and the treatment is difficult. 

Lumbar Neuralgia. True essential neuralgia of the lumbar nerves 
is so rare that it may be almost laid down as an axiom that pain in 
them means neuritis or inflammatory and neoplastic development in 
and about the pelvis. 

Sciatica I regard practically as always a neuritis or a mere sec- 
ondary pain. I will discuss this further under the head of the sciatic 
nerve. 

Pains that appear in the lower abdominal region, in the scrotum. 
along the perineum, in the buttocks and down the thighs will almosl 
surely be found associated with some pelvic disease. 

Coccygeal Neuralgia. Coccydynia. This is practically a woman's 
disease. It is an intractable neuralgia of the coccygeal plexus and 
interferes with sitting. It may be excited by walking or evacuation 
of the bowels. It is sometimes associated with a local inflammation, 
though usually it seems to be an idiopathic neuralgia. ( Opiates by 
Suppository, local irritants and finally operations have had to be resorted 
to. Electricity has often here proved effective, one pole being placed 
over the coccyx and the other in the vagina. 



252 



THE NEURONIC DISEASES 



Plantar Neuralgia. Pododynia. The pain here is in the heel and 
sole of the foot. 

Visceral Neuralgias. These occur in neurasthenic and hysterical 
women, especially in connection with the heart and the stomach. They 
must not be confused with the crises of tabes and other forms of symp- 
tomatic visceral pains. Pelvic neuralgia is very common in women. 
There is a nephralgia that may even lead to operation for renal calcu- 
lus. The intestines, the liver, the spleen may possibly be the seat of 
pure neuralgia, but if so it is very rare. These pains usually mean 
some organic disease and had better always be regarded in that light. 

Spermatic neuralgia is a very rare but obstinate affection. 

Urethrodynia is a rare and obstinate trouble. 

ECLAMPSIA. 

Convulsions that resemble epileptic fits, that tend to recur, and that 
are dependent upon causes outside of inherent brain changes, are now 
specifically designated by the term eclampsia. From one point of 
view they may be looked upon as a sort of symptomatic epilepsy, but as 
they are always acute and in most cases cease entirely after a short 
time, or after the removal of the cause, it is well to use another name 
for them than that of epilepsy. 

There are three prominent types of eclampsia which should receive 
some notice in a volume upon neurology — namely, infantile eclampsia 
(eclampsia infantum), parturient eclampsia (eclampsia parturientium) 
and ursemic convulsions (eclampsia urcemica). 



ECLAMPSIA INFANTUM. 

During their early years children are very subject to convulsive 
seizures upon various provocations. It has been suggested that this 
is due to the immature and undeveloped condition of their nervous 
apparatus, especially the w r eak condition of the higher inhibitory cen- 
ters, a reason which has some plausibility in it, but fails to account for 
the convulsions of childbed and ura?mic poisoning. 

Etiology. — The causes of infantile convulsions are numerous, 
though they may all be grouped under any one of the three heads, 
reflex, infectious and psychic. Rickets and general debility are very 
important factors in the production of the trouble. Just how much is 
to be attributed to the cachexia itself, and just how much to the various 
disturbances which the cachexia leads to, it is not easy to say. Rickets 
occurs chiefly between the sixth and eighteenth months of life. It is 
a condition that fosters or represents defective development just at 
the period when the development normally is most active. As a result 
it leads to bad dentition, to gastro-intestinal irregularities and to de- 
fective nutrition generally. A rickety child as a rule will exhibit a 
large number of local malformations and functional abnormalities. 
These-, taken in conjunction with the general defective nutrition, con- 
stitute a long list of causes of infantile convulsions. The laity always 
think of worms first among the possible causes, but they are not such 



THE NEURONIC DISEASES 253 

frequent factors as auto-intoxication from gastro-intestinal defects, 
the distress of difficult dentition, overloading of the stomach, especially 
with indigestible food, profuse diarrhoea, etc. Phimosis, otitis media, 
inguinal hernia and other sources of peripheral reflex of an abnormal 
character acting upon a badly nourished and undeveloped brain, mav 
all be counted among the causes. 

Infectious fevers very frequently start in children with a convul- 
sion. It is probably of the same nature as eclampsia now under consid- 
eration, though as a rule it is not regarded as the same. It is thus seen 
in scarlet fever, measles, pneumonia, etc As a symptom of brain dis- 
ease, congestion, inflammation, hydrocephalus or meningitis it must be 
remembered. Natal hemorrhage may induce a convulsion immediately 
after birth, to be followed later on by all the usual sequelae, such as 
hemiplegia, epilepsy and mental deterioration. Mental shock, such as 
fright, night terror, fear upon being suddenly left alone, has provoked 
convulsions. 

No case of infantile convulsions should be regarded lightly, for be- 
sides indicating a dangerously susceptible, possibly cachectic, constitu- 
tion, it may be but the first indication of genuine epilepsy. -Out of 1,450 
cases of epilepsy Gowers found that 180 began within the first three 
years of life. Osier analyzed 460 cases of epilepsy in children and 
found that in 187 the fits commenced within the first three years. This 
is the period of life in which eclampsia occurs. As a rule epilepsia con- 
tinues on past the period, whereas eclampsia ceases. Such, however, 
is not always the case. Convulsions have occurred in infancy and epi- 
leptic fits later in life. It would be desirable to know just what is the 
exact relationship between epilepsy and eclampsia, if there is any. It 
certainly is not true that early convulsions produce later epilepsy. 
Hysteria has occurred in adults who had convulsions in childhood. It 
seems more likely, therefore, that a neuropathic constitution is present, 
which yields easily in childhood to causes that provoke a convulsive 
seizure, but is able to resist the greater neurosis until a later age. Epi- 
lepsy as we have seen occurs in infancy. It is the mistaking of these 
cases for eclampsia that makes every case of the latter disease a mat- 
ter of serious consideration. 

Symptoms. — These are much the same as those of epilepsy. Pre- 
monitions are sometimes seen in an excessive irritability, with facial 
changes, slight twitchings about the mouth and rolling of the eyes. 
Most mothers can detect an oncoming convulsion when others see noth- 
ing wrong. The attack usually appears suddenly with fixation of the 
eyes, pallor of the lips and face, stiffening out of the trunk and ex- 
tremities, rotation of the head and disturbed respiration. The fit is 
epileptiform in every respect, except in its severity. In a minute or 
so the spasm relaxes, not to appear again for some minutes or an hour 
•or so, or it passes into a clonic condition which is usually slight and in- 
volves the face, eyes, hands and feet. In other cases, a moderate tonic 
spasm, interfering somewhat with the breathing, may continue for 
twenty or thirty minutes. Sometimes a series of brief convulsions oc- 
curs with partial recovery only in the intervals. A scream accompanies 
some of the attacks. In other cases only screaming, grinding of the 



254 THE NEURONIC DISEASES 

teeth and a slight bilateral rigidity are observed. These convulsions- 
are to be distinguished on account of their bilaterality from the hemi- 
plegic spasm of brain lesions. 

( rradually the attack subsides, and the child goes to sleep in a state 
of more or less stupor. In fatal cases the attacks are severe and run 
together in rapid succession, coma being present as the child dies. 
1 )eath is particularly to be dreaded in weak children, in cases with great 
frequency of the attacks and in diarrhceal hydrocephaloids. 

Eclampsia usually ceases after a time never to recur. If the con- 
vulsions continue on throughout the second, third and fourth years they 
must be looked upon as being epileptic. They are also epileptic if they 
do not cease after the removal of what may be regarded as an obvious, 
possible cause. 

Diagnosis. — The chief differential diagnosis always to be made is 
between eclampsia, epilepsy and organic brain disease. The first comes 
on suddenly in a state of relative good health, is associated with some 
obvious cause, disappears with the removal of the cause and does not 
continue or recur later on. The second continues after having once 
appeared, in spite of the removal of apparent cause, and in every way 
more nearly represents a true epileptic than does the eclamptic seiz- 
ure. The third reveals characteristic organic symptoms, one-sided 
spasms that are more or less permanent, and other signs of intra- 
cranial hemorrhage, meningitis, etc. Laryngismus stridulus, rickety 
spasms and rigidity, and the hydrocephaloid state have all an eclamptic 
appearance but need not be considered here further. 

Prognosis. — This is always serious. Some children are able to 
pass through the ordeal, but weak and debilitated infants usually suc- 
cumb. Infant mortality is largely dependent upon eclampsia. Febrile 
convulsions are not very serious but as I have said they are regarded 
by some as not exactly the same as eclampsia. They usually occur in 
more robust children. Chronic diarrhoea with eclampsia usually means 
death. The prognosis also takes in the question of the seizures being 
those of genuine epilepsy. After the third year eclampsia is practically 
never seen. 

Treatment. — Remove causes that can be removed and treat those, 
like the rickety condition, in the usual way with syrup of the iodide of 
iron, cod-liver oil, hypophosphites, etc. Every mother knows the value 
of sudden immersion in a warm bath. Bromides, chloral and chloroform 
inhalations are available means for controlling the spasms. Morphia 
hypodermically, or nitrite of amyl may have to be tried in an attack. 
Bromides can lie continued afterwards. 

ECLAMPSIA PARTURIENTIUM. 

Etiology. — Young primiparae are the most frequent subjects of 
childbed convulsions, though women of all ages and with any preg- 
nane) may have them. They usually occur in the last two or three 
months of pregnancy, during the parturient act or soon after it. Many 
of the- patients are epileptics and the convulsion is only one of their 
usual tits. \ arious opinions used to he held in regard to the real cause 



THE NEURONIC DISEASES 



255 



of these convulsions such as reflex irritation in the womb, sepsis and 
cerebral anaemia from the loss of blood. All authorities agree nowadays 
that nephritis is the cause and that the convulsion is really uraemic. It 
is true that the coma of uraemic eclampsia is usually wanting in puer- 
peral eclampsia, whereas in the latter some credit must be given for 
the reflex influence from the uterus ; the statement is not therefore 
weakened that both uraemic and parturient eclampsia are due to the 
same cause and are therefore all but identical. Albuminuria, oedema, 
amaurosis and albuminuric retinitis may all be present and confirm the 
etiology. Infection may play a role in some cases from a specific 
bacillus. 

Symptoms. — These resemble an epileptic seizure in every respect. 
In addition there are uraemic manifestations such as intense headache, 
precordial pain, sudden blindness and oedema. The fit sometimes in- 
cludes a scream, profound coma, pallor, biting of the tongue, fixation or 
rolling of the eyes, and violent general tonic and clonic convulsions. 
The temperature often rises, the pulse becomes weak and the respira- 
tions assume the Cheyne-Stokes character. 

Prognosis. — About thirty per cent, of the cases die in coma, in 
an apoplectic attack or from the sepsis. Status epilepticus with a tem- 
perature of 109 degrees has destroyed some patients. 

Treatment. — To hasten the delivery, and how best to do it, 
are questions entirely for the obstetrician. Venesection that used to be 
so frequently practiced is now regarded as contraindicated. It weakens 
the patient merely, without modifying the source of the trouble in the 
kidneys. Chloroform inhalations, morphine, chloral hydrate in full 
dosage, venesection with transfusion, diaphoresis with vapor baths 
and pilocarpine, and free purgation are all to be resorted to according 
as the demands of the case and the vigor of the patient will indicate. 

ECLAMPSIA UR/EMICA. 

The cause of this is of course nephritis. The presence of the kid- 
ney disease is determined by the condition of the urine, albumin and 
casts being generally present, by the hypertrophy of the heart and by 
the albuminuric retinitis. Just what is the mechanism by which the 
state of blood under these circumstances causes coma and epileptiform 
seizures is not entirely clear. 

The convulsions usually occur suddenly though there may be 
some headache, restlessness, visual disturbances, twitchings of the mus- 
cles, even a comatose state and visual obscurity just before their onset. 
I have seen such symptoms in patients in whom I could only diagnose 
a renal insufficiency, and have observed them disappear with the free 
use of cathartics and diuretics. They certainly suggested a remote re- 
semblance to uraemia of mild degree. 

May not some of the cardiac irregularity, the pains, die general 
irritability, the fibrillary muscular twitchings of some severe cases of so- 
called neurasthenia be due to slight renal trouble, enough to provoke 
a faint degree of uraemic intoxication ? 

In typical uraemic convulsions the coma, the spasms, tonic and 



256 THE NEURONIC DISEASES 

clonic, the biting of the teeth, the rolling of the eyes are all clearly 
epileptiform. Nystagmus is sometimes present. The pupils are gen- 
erally dilated and fail to react to light. They have been seen contract- 
ed for a brief spell and then dilated. Respiration is greatly embarrassed 
and right after the fit the knee-jerk is gone. Coma, sleep or drowsi- 
ness may all follow the fit. 

Treatment. — Purgatives and hot baths should be used when an 
attack is threatened. The bowel may be irrigated with water at a tem- 
perature of 150 degrees F., and nitroglycerin freely used. For the seiz- 
ure chloroform inhalations must be used, and morphine and chloral. 
Purgation, diaphoresis, with hot applications and pilocarpine, and mor- 
phine especially for the delirium are about all that can be done. 

TETANY. TETANILLA. 

This is a disease characterized by tonic, intermittent or continuous 
spasm of symmetrical distribution in the ends of the extremities ; by 
certain indefinite and irregular sensory and general phenomena; and 
by a causation that points strongly in the direction of a severe intoxi- 
cation of the spinal cord or lower neurones. Our knowledge of its 
pathology is not ample enough yet to enable us to classify the disease 
definitely. It is seen but rarely in this country. In Europe it is more 
common and in some places of Sweden and Austria appears to be 
almost endemic. It has occurred epidemically in the spring of the year. 
The first account of it was given by Steinheim and Dance, but it was 
through the work of Trousseau that it first became generally known. 
Many investigators have studied it carefully since, but their views are 
still unsettled and divergent. It has been called pseudo-tetanus, essen- 
tial contracture, and shoemaker's spasm. 

Etiology. — Tetany has been seen in every period of life. It is 
most frequent, however, in early childhood and in early adult years. Up 
to the age of about twenty males are far more subject to it than fe- 
males. After twenty, strange to say, the number of females is almost 
double that of the males. This argues emphatically against an occu- 
pation cause for the disease so strongly believed in by many. Children 
and girls are physically nearer together than are either to adult males. 
After fifty the males begin to predominate again. Occupation per se 
is hardly a cause of the disease though it is said that forty-three per 
cent, of the cases occurred among shoemakers in the German epidemics. 
The chances are that contact with some poison is favored by the hand- 
ling of leather. Certainly the disease is not the occupation neurosis 
known as cobbler's cramp. 

The toxic, infectious origin of the trouble is all but positively sug- 
gested by a large number of etiological factors. When it occurs in 
women, for instance, it is usually about the particularly exposed periods 
of pregnancy and lactation. It is seen in connection with many gastro- 
intestinal troubles, so that a gastric tetany is often spoken of. Diar- 
rhoea, intestinal parasites, constipation, the use of tainted food and 
pyloric stenosis with dilatation of the stomach have preceded it with 
suspicious frequency. One woman suffered immediately after eating 



THE NEURONIC DISEASES 257 

some grapes and drinking soda water. Diarrhoea is a particularly com- 
mon antecedent in children. Autointoxication is probably the explana- 
tion of these cases. 

It is fostered by all depressing influences such as exposure to cold, 
fatigue, acute disease, rachitis and other diathetic and cachectic con- 
ditions. Be the factor what it may, if it exhausts and debilitates the 
constitution in general it favors the onset of tetany. Some of the gas- 
tric cases have been supposed to be reflex in character because the 
spasm appeared immediately upon the introduction of the stomach- 
pump. Why does it not occur more frequently then under such condi- 
tions, if it is a reflex and not a toxic disease? Cessation of the spasm 
by removal of intestinal parasites does not argue for the reflex any more 
than it does for the toxic hypothesis. In favor of the latter is the oft- 
observed fact that extirpation of the thyroid gland is followed by it. 
It was seen soon after the injection of spermine. Nephritic disease, the 
use of alcohol, ergotin and chloroform, the finding of toxic substances 
in both the stomach and the urine, are data enough to almost establish 
the toxic origin of the trouble. 

Among the infections that it has accompanied may be enumerated 
typhoid, scarlet fever, rheumatism, measles, diphtheria, malaria, influ- 
enza, pneumonia and smallpox. Generally the spasm appears during 
the convalescence from these diseases. 

Whether there is any special significance in the rather frequent 
association of hysteria and epilepsy with tetany it is doubtful to say. 
The question is one of importance from the standpoint of differential 
diagnosis rather than of etiology. It is easily conceivable that a type 
of constitution that tends toward the instability of hysteria and epi- 
lepsy would easily yield to a toxic irritant and present the clinical pic- 
ture of tetany. 

Pathology and Pathogenesis. — Nothing distinctive in the way 
of morbid anatomy has been found. Some poliomyelitic changes may 
or may not be due to the reaction upon the cord of the violent muscu- 
lar contractions. The same changes have been recorded in connection 
with other virulent intoxications involving the cord and lower neu- 
rones, as witness acute ascending paralysis of the Landry type. Hypere- 
mia and small hemorrhagic foci have been seen, with accumulation of 
lymphoid cells about the capillaries, and even minute spots of myelitis. 
The ganglion cells have been swollen or shrunken, cloudy and softened 
and full of vacuoles. In other words chromatolysis has been present. 
The spinal membranes, especially in the cervical region, have been con- 
gested. All of these occasional findings are too indefinite to establish a 
fixed pathology upon, but when we compare them with the similar 
findings of other forms of severe intoxication, particularly Landry's 
disease and some cases of alcoholism, we are impressed with the fact 
that if tetany be indeed a functional disease, a functional disease is not 
always one without any organic change whatever. Whether the spasms 
preceded or followed the few organic changes that have been observed 
is immaterial in comparison with the suspicious fact that the two phe- 
nomena are actually associated together. The association alone ren- 
ders very shaky the rather paradoxical notion that functional exhibi- 



258 THE N ELKO N 1 C DI SEA SES 

tions can be existent without some structural, molecular or chemical, 
change. 

Until we get more positive data, it may be well to still speak of 
tetany as a functional disease and classify it among the neuroses. That 
the trouble is probably a toxic disturbance of the nutrition of the cells 
in the spinal cornua is suggested by the symmetrical character of the 
symptoms showing a central seat for the lesion, by the prominence of 
the motor manifestations over the sensory, by the similarity of the clin- 
ical picture in some respects to ergot and strychnine poisoning, and 
by the few poliomyelitic post mortem findings. 

The subsequent atrophy in the spinal cells seen in some rare cases 
and the almost total absence of inflammatory signs, suggest that the 
tn ul>le is a toxic primary neuronic degeneration. 

Symptoms. — The characteristic symptom of tetany is the muscular 
spasm . There may be sensory phenomena of an indefinite character 
and same other general disturbances. The mind is never affected. 

There may be premonitions of the disease but they are not com- 
mon. Usually they are of the constitutional and sensory type. Among 
them are a feeling of malaise, apathy, headache with nervous vomiting, 
pains in the back and down the limbs. Sometimes just before the spasm 
appears, various paresthesias will be felt, such as tingling, pins-and- 
needles sensation, burning and numbness in the extremities. At length 
the upper limbs, particularly the fingers and hands, more rarely the 
lower limbs, exhibit a condition of tonic spasm. Sometimes the feet 
are affected at the same time. The trunk is very rarely involved. So 
characteristic is the attitude of the hands that the disease can be diag- 
nosed from it alone. 

It is to be noted that the spasm is tonic and that it is symmetrically 
distributed. The appearance of the hand is much like that of one writ- 
ing. The ends of the fingers are pressed together and inclined toward 
the ulnar side. The thumb is strongly adducted and partially flexed 
beneath the index finger. The palm is hollowed and the wrist is some- 
what flexed. The condition of the fingers is due to flexion at the 
metaearpo-phalangeal joints and implication of the interossei muscles. 
Very rarely has extension of the wrist and fingers been observed. In 
the foot the ankle joint is extended, the toes flexed and overlapping, 
and the attitude that of equino-varus. The knees are generally extended 
though they may be flexed, and the thighs are occasionally adducted 
and flexed. 

This spasm may be intermittent every few minutes or hours or 
days. Sometimes it lasts many weeks. It can be provoked by irritation. 
The muscles are and feel rigid. Attempts to move them passively 
usually cause pain. Of course their condition interferes with all use 
of the hands or renders the movements and gait awkward and difficult. 
The strength of the contractions varies between wide extremes. It may 
amount to a slight stiffening or an immovable tetanic contracture. In 
the intervals the sensitiveness of the parts, and even the paresthetic 
sensations, usually continue somewhat. They rarely disappear entirely 
with, or as promptly as, the spasm. 

Other muscles besides those of the limbs may be involved. In 



THE NEURONIC DISEASES 



259 



the severe cases all or any of the muscles of the body may be thrown 
into a state of rigidity. Swallowing and respiration may be interfered 
with. The ocular muscles have been affected and nystagmus has been 
noted. 

- FIGURE 40. 







& 




Position of the hands in tetany. (After Oppenheim.) 

The patient's consciousness is not, except in the rarest instances, 
altered. 

The temperature and pulse rate during the attack are usually 
somewhat elevated. At other times they have been seen to be sub- 
normal. 



I UK NEURONIC DISEASES 

The electrical phenomena of tetany are remarkable and some- 
times unique. They are usually referred to as Erb's sign. There is an 
exalted degree of excitability of the nerves to both the faradic and 
galvanic current. With the latter there is a complete reversal of the 
polar reactions to a remarkable degree, cathodal closing contraction 
equaling, and in rare instances even surpassing, that of anodal clos- 
ing. In the average case, only a weak current is required to produce 
a cathodal closing contraction. The current that would be needed in 
health to cause this response, produces in tetany a violent tetanic con- 
traction. Anodal opening tetanic contractions and cathodal opening 
tetanic contractions may be provoked. The latter is never seen in any 
other disease than this. For the sake of brevity, these reactions may 
be represented by and compared with the normal formulae, thus: 

Normal— CaCC, An CC, CaOC, AnOC. 
Tetany— AnCC, AnOC, CaCC or AnOC, AnCC, CaCC, AnOTe. 
\n( )TE and CaOTE are never seen in any other disease in man. 

Along with this electric hyperexcitability there is an increase of 
the mechanical irritability. As Chvostek's sign it consists of a vigor- 
ous contraction of the muscles, especially those of the face, when the 
relate;! nerve is slightly tapped or irritated. Trousseau's sign is prob- 
ably due to the same mechanism. It consists in provoking the spasm 
by compressing the nerve trunks or bloodvessels in the limb in such 
a way that the arterial or venous blood is impeded. Trousseau's sign 
is not observed in any other disease, though Chvostek's has been seen 
in tuberculosis and simple gastric dilatation, but less marked than in 
tetany. 

Increase of sensory excitability to both mechanical and electrical 
stimulation is known as Hoffmann's sign. That the sensory nerves 
are hyperaesthetic is shown by the radiating paraesthesia that occurs 
in their areas of distribution when they are compressed. The supra- 
orbital, ulnar and major saphenous nerves are available for this test. 
Chvostek noticed the phenomenon in connection with the auditory 
nerves, these nerves reacting to comparatively weak galvanic currents, 
whereas in health only about fifteen per cent, of cases react and then 
only to strong currents. A clang is observed upon anodal closing, 
when the anode is held still, and upon anodal opening. 

What Bechterew calls the reaction of excitation is the progressive 
increase of the mechanical and electrical excitability by repeated stim- 
ulation. 

( )ther inconstant symptoms are met with. The association with 
hysterical and epileptic manifestations has already been noticed. 
Myxcedema and exophthalmic goitre have been seen with it. Even 
psychic disorder with hallucinations and confusion have been noted as 
in other similar toxic diseases. Some of the vasomotor and trophic 
exhibitions are quite prominent at times. Hvperidrosis, polyuria, 
albuminuria, glycosuria, cedema, urticaria, herpes, pigmentation and 

of hair and nails have all been recorded. 

There is nothing of moment in connection with the reflexes. Sev- 
eral times the knee-jerks were lost. 

Incipient cataract, believed b\ Peters to be due to obstruction of 



THE NEURONIC DISEASES 26l 

the circulation near the lens from spasm of the ciliary muscle, mydria- 
sis and pupillary rigidity are among the occasional ocular symptoms. 

General chilliness, fugitive pains, nausea, vomiting, diarrhoea, in- 
crease of temperature and pulse rate are seen in the beginning of the 
trouble, and even later, and are probably mere evidences of the general 
intoxication. 

Diagnosis. — The clinical picture is so unique in fairly typical cases 
that there ought to be no difficulty in arriving at the diagnosis. The 
attitude, the intermittent tonic symmetrical contractions in the hands 
and feet, the electrical signs, the probable history of infection or intoxi- 
cation, should all be given due consideration. Even when the spasm 
appears in the muscles of the jaw, trismus, tetanus can be differen- 
tiated by the fact that in tetany the trismus is a later phenomenon, the 
spasms are intermittent, and are more marked in the extremities than 
they are in tetanus. In the latter the extensors, supinators and adduc- 
tors are more apt to be affected ; in tetany the flexors, pronators, ab- 
ductors and internal rotators. The finding of the tetanus bacillus 
clinches the diagnosis. 

Latent tetany of childhood, tetany without spasm but with parges- 
thesia, Erb's and Chvostek's signs, and even a pseudo-tetanus of in- 
fancy have been noted. 

The differential diagnosis between tetany and spinal meningitis, 
hysteria, epilepsy and torticollis is not difficult if the characteristic 
electrical and other signs of the former are conscientiously sought for 
and the symptoms other than the motor are inquired carefully into in 
the latter. 

Prognosis. — In most cases the prognosis as to life may be re- 
garded as favorable. Bad signs may develop suddenly, however, at 
any time. Therefore, the cases are always serious. The accompani- 
ments of the disease vary the prognosis. Thus in cases with gastric 
dilatation, in those in which a goitre has been cut out, in those sub- 
jects exhausted and debilitated by disease and where respiratory com- 
plications are present, it is grave. Delivery and the cessation of lacta- 
tion usually terminate these forms of the disease. Infectious and intox- 
icating cases frequently run a mild and rapid course to recovery. Some- 
times the recovery is tardy and relapses are not to be unexpected, es- 
pecially when pregnancy and the function of lactation recur. The 
course of the entire disease may be from a few days to many months, 
even, without remissions, to many years. 

Treatment. — All possible causes and irritants should be removed 
as promptly as possible. Intestinal entozoa should be gotten rid of, the 
foetus should be delivered, tainted food should be washed up. The 
termination of the pregnancy in the pregnant cases, and the adminis- 
tration of thyroid extract in the absence of the thyroid gland, usually 
cause a disappearance of the disease. 

For the rest, we must depend upon rapid elimination, diaphoretic 
treatment in cases following cold, and the use of nerve sedatives. Free 
diuresis, catharsis, and diaphoresis cannot certainly be as dangerous 
as the disease itself is. Bloodletting is hardly commendable, or the 
icebag to the spine either, in view of the high probability of the dis- 



262 I HI". NEURONIC DISEASES 

ease being a general toxaemia. The stomach pump cannot be used 
and in all manoeuvres the danger of provoking spasm must always 
be remembered. Warm baths and warm wet packs are both sedative 
and eliminative. 

Of the sedatives potassium bromide is the most available. It must 
be given in full dosage, 30 to 60 grains, three times a day. For a 
severe and extensive paroxysm morphine may have to be used. It 
cannot be employed continuously, however, for obvious reasons. It 
is in the continuous cases that the bromide salt is applicable. Hyoscin 
hydrobromate, gr. T-25, hypodermically every hour, until full medic- 
inal effect is obtained, has helped in some cases. Curare and curarine 
and phosphorus have their advocates. Sanger Brown has been pleased 
with the use of chloral and chloroform narcosis. When the laryngeal 
and respiratory muscles are threatened, chloroform inhalations are 
especially to be recommended. Administration, of course, must be 
careful, especially in the beginning. Pilocarpine subcutaneously will 
also temporarily relax the muscles. Look out for exhaustion and do 
not carry the use of either chlorofrm or pilocarpine too far. 

One wonders how electricity had ever been thought of as a thera- 
peutic agent in such a disease, and yet a stabile, mild galvanic current 
has the approval of good authority. The faradic current is decidedly 
contraindicated. 

General tonics like iron, quinine and cod-liver oil should be given 
between paroxysms, especially in children. 

Moynihan urges the early adoption of surgical measures in cases 
of severe gastric tetany, which certainly seems reasonable when there 
is a mechanical impediment to the free working of the organ from 
pyloric stenosis. 

LOCALIZED MYOSPASMS. 

A spasm is a symptom. It is an involuntary and abnormal con- 
traction of a muscle, due to disease. It arises out of a multitude of 
conditions involving the entire neuro-muscular apparatus. 

Spasms may be classified upon an anatomical or a functional 
basis. As the anatomy and functions of the entire neuro-muscular 
apparatus are very extensive and complex it is obvious that such clas- 
sification must prove chaotic and confusing. This is just 
the condition of most of the classifications of this symptom 
at the- present day. And it can hardly be expected to be 
improved very much until we learn more of the patho- 
logical origin of the trouble. It is uesless to form a classification with 
such gn i.ss anatomical divisions as the head, the neck, the trunk and 
the. extremities for its guiding principle, for spasms in one part are 
very generally accompanied b) spasms in another part. It is generally 
futile to classify them in accordance with the particular nerves involved, 
for not always are the same nerves implicated nor is the spasm always 
a nerve trouble. In the production of a muscular contraction many 
structures are concerned. They are the muscular tissue itself, the 
neuraxone, the motor neurone-cell and under most circumstances the 
related sensory neurone with all its peripheral connections. In the 



THE NEURONIC DISEASES 263 

voluntary and semi-voluntary muscular contractions the centers that 
subserve volition and the other higher psychic acts must also be taken 
into account. Thus it is clear that a normal muscular contraction is 
by no means a simple affair. Disorder of any part of this complicated 
mechanism may very reasonably provoke a disorder of the resulting 
contraction which may assume the character of an over-contraction. 

Direct irritation and withdrawal of inhibition are the two forms 
in which the primary disorder occurs out of which the spasm is evolved. 
The irritation may be in the muscular or the nervous part of the mech- 
anism. Disease of the brain and other inhibitory centers may cause 
certain sensory-motor mechanisms to be set free, as it were, to func- 
tionate in a manner far in excess of the normal. It is not correct, there- 
fore, to say that spasm is a symptom of spinal cord disease. It may 
be a symptom of disease in any part of the sensory-motor neuro- 
muscular apparatus. This at once suggests that these spasms might 
be classified into those due solely to muscular disease and those due 
to nervous disease. The latter could again be subclassified into those 
that are dependent upon lesions in the motor, the sensory or the cere- 
bral centers that subserve psycho-motor-sensory functions. We 
already use this classification for some of the spasmodic manifesta- 
tions and were we in possession of complete data m regard to all of the 
diseases in which they appear we would probably find that this classi- 
fication would prove the best. We distinguish even now between the 
spasmodic conditions of cerebral irritation and cerebral destruction. 
We recognize in our nosology a whole host of sensory reflex spasms. 
We acknowledge that psychic spasm may occur in hysteria and allied 
states. In a word we have conceived of an anatomical basis for most 
of the spasmodic conditions that we meet with. For want of a better 
term we call these spasms sometimes symptomatic, which means 
merely that we are fortunate in knowing just about what the lesion is 
that is causing all the trouble. These spasms being but symptoms of 
well recognized diseases it does not seem to me necessary to describe 
or refer to them again in this chapter. They will be found treated in 
detail under the head of the respective diseases wherein they appear. 

The spasms of which we have as yet no definite knowledge in re- 
gard to their pathogenesis but which are well recognized clinically will 
be considered here. 

For physiological reasons already spoken of, it will be assumed 
that in these spasms there is a functional disturbance which may in- 
volve the muscular tissue or the central neurone-bodies. The term 
functional has a broad meaning here. It may be allowed to indicate 
a nutritional, or at least, a physio-chemical, change of some sort in 
these elements or a disturbed innervation among them whereby they 
permit of unrestrained activity in the muscles. 

From this point of view the spasm that is not due to inherent mus- 
cular disease is a primary neurosis. In these spasms heredity, <>r in 
other words the neuropathic constitution, nutrition, infection and trau- 
mata play the largest etiological role. 

These spasms may be at times excited by reflex stimulation but 
they are not pure reflex spasms. They are generally accompanied by 



j(,4 I HE X ILL' RUNIC DISEASES 

other signs of a neuropathic state and very often by another distinct 
neurosis like hysteria or neurasthenia. 

In taking up for consideration then those spasms that are them- 
selves of the nature of pure neuroses, I discard all those that are 
symptomatic of, or form merely a part of, the symptom-complex of 
well-recognized diseases discussed in other parts of this book. I realize 
the risk I am running in possibly including here some spasmodic 
affections that may be merely symptomatic, but the uncertainty of our 
knowledge as to their real nature may serve as my apology for taking 
the step. 

These spasms may be regarded from the standpoint of their clin- 
ical appearance, which is useful incidentally for purposes of descrip- 
tion but which should never have been adopted as a basis for classi- 
fication as it unfortunately too often has been. They will be spoken of 
as tonic and clonic, as belonging to this group or that group of mus- 
cles, as rapid or slow, as coordinated or incodrdinated, as involving 
parts of the muscles or the whole muscle. 

Walton rightly urges that a more careful use of terms in describ- 
ing these spasms should be insisted upon. By way of illustration he 
recommends that the term myoclonia should be dropped as a collective 
designation for unrelated disorders, in which I heartily agree with 
him, and that myokymia should be limited to cases showing, without 
hereditary or congenital history, widespread muscular quivering with- 
out indication of progressive degeneration of the nervous system, with- 
out constitutional symptoms and without signs of present infection 
or other acute disease. And so on. 

It is not possible in the present state of our knowledge to always 
separate an essential myospasm from one due to some functional or 
other nervous trouble, any more than it is possible to separate an es- 
sential progressive muscular atrophy from a low grade chronic anterior 
poliomyelitis. It is not improbable that we will come to believe, as 
many are believing in regard to the atrophy and anterior horn trou- 
ble, that there is no sharp line of demarkation ; that functional muscu- 
lar disturbance is always more or less accompanied by a related neural 
trouble. 

L( >CALIZED SPASMODIC TIC. TIC CONVULSIF. 

A quick, sharp, short, electric-like, painless contraction in a muscle 
<>r group of muscles is known as a spasmodic tic. It may occur in any 
muscle of the body, though it is most frequently seen in the facial mus- 
cles, probably because they are the most active and intimately con- 
nected with mentalization of any in the body. 

\ tic may consist o\ one contraction. Usually there are several 
in rapid succession, after which there follows a period of quiescence. 

Sometimes a single nerve is involved or even single branches of 
a nerve. \\-r\ often, however, a number of nerves, nearby or widely 
separated, may be subject to the trouble. As a result different mus- 
cles, but always muscles concerned in the production oi related move- 
ments, an- contracted. 



THE NEURONIC DISEASES 265 

The disease is a chronic disorder, has usually a neuropathic his- 
tory behind it, and occurs frequently in association with hysteria, epi- 
lepsy, and other neuroses and psychoses. 

A nutritional or molecular change of some unknown character in 
the nerve nucleus or its representative center in the cortex is assumed 
as the pathological basis of the trouble. 

These localized tics are often miscalled local or habit chorea. 
They have nothing in common with the latter disease and the manner 
of the muscular movements is not the same. 

The tics should always as far as possible be sharply differen- 
tiated from mere reflex and symptomatic spasms of the same muscles. 

The results of their treatment respectively are very different. The 
tics are not very amenable to treatment and in their management dis- 
ciplinary and psychotherapeutic measures have a large share. They 
represent a fundamental, hereditary, general nervous defect or the neu- 
ronic, residual change after the operation of some acute cause or dis- 
ease. They speak always for more or less central degeneration and 
are therefore apt to be of wide distribution or concerned with mus- 
cles and nerves that subserve general physiological movements. They 
may, however, implicate individual muscles and nerves. 

The facial tics are the most common and most marked. The rea- 
son, as I have said, is because the facial reflexes are so rapid and so 
closely linked with mentalization. The psychogenic origin of them in 
many instances is shown in the way that they suddenly begin after 
a high emotion or mental shock. Most of the victims are more or less 
mentally undergrade, or are at least neuropathic. A vicious habit may 
evolve the trouble. The trouble is only very rarely obtained by direct 
inheritance. They may resemble and even originate as an occupation 
neurosis. I saw such a tic that occurred in a young cornetist with 
both a family and an individual pronounced neuropathy. Any of the 
muscles of the face may be affected, and the symptom may be bilat- 
eral, though it is usually unilateral. Single muscles and groups of 
muscles may be involved. Perhaps the most frequently affected is 
the orbicularis palpebrarum and the least the orbicularis oris. Tn 
fact there is no rule and every possible form of the exhibition may be 
looked for. The occipito-frontalis, the chin muscles, even the external 
auricular muscles have each been seen to be affected by themselves. 
Both tonic and clonic have been the contractions, though the latter 
are the more usual. Mental and physical rest diminish the jerks, 
whereas excitement, effort and voluntary movements increase them. 
Cutaneous irritation usually evokes them. Sometimes they can be par- 
tially controlled by the wili. These spasms do not impair much the 
ordinary voluntary movements of the face, and as a rule they do not 
cause much subjective distress, sometimes not any. Hearing phe- 
nomena may occur when the stapedius muscle is affected. The velum 
palati and uvula have been supposed to be implicated, though these 
are more likely to be due to some gross organic lesion which may be 
diagnosed by collateral symptoms . There are no sensory, vasomotor, 
trophic or secretory symptoms. The objective signs, except the eon- 
tractions, are all negative and the trouble appears to be a pure neurosis. 



266 



THE NEURONIC DISEASES 



Of course every case of facial spasm is not a pure tic. Organic 
lesions of the nerves and their representative centers may cause facial 
spasm. Such cases must be always differentiated and in every case 
it is well to hunt first for some such organic cause. Tic patients are 
often the victims of hysteria, epilepsy, hemicrania, hystero-neuras- 
thenia and the psychoses. Stuttering is usually a form of tic, though it 
may have had its origin in a vicious habit. Tic may be spoken of as 
mimic tic but it is entirely wrong to name it chorea as is so often done. 

Facial tic is a chronic, sometimes remittent trouble, with a gen- 
erally unfavorable prognosis as to cure. Blepharospasm holds out the 
most hope of amelioration. 

No treatment but general tonic and disciplinary treatment will do 
any good. I have seen arsenic cause a bad blepharospasm in a boy 
almost entirely to disappear for a time. Bromides may help some. All 
other remedies usually fail. If the spasm be not a true tic, but a nerve 
reflex or symptomatic trouble, the treatment is both obvious and prom- 
ising. If tic douloureux be present with the motor tic it must be 
treated as a separate condition. 

A masticatory tic is sometimes seen that involves the muscles of 
mastication supplied by the motor branch of the fifth nerve. Trismus, 
hysterical, rheumatic and reflex spasms of the lower jaw must all 
be carefully differentiated. The reason that the prognosis of most of 
the cases of masticatory spasm is favorable is that they are not cases 
of true tic but are due to inflammations about the temporo-maxillary 
articulation, to diseased teeth, to hysteria, etc. 

What is said of masticatory tic is true of occasionally observed 
hypoglossal tic. The tongue here shoots rapidly in and out of the 
mouth, or from side to side.- The spasm is generally bilateral but a 
hemispasm has been seen. A tremor in the glossal muscle and the 
spasm of some neighboring facial muscles have accompanied this tic. 
Alternation of masticatory and hypoglossal tic is a curious phenome- 
non. Sometimes the trouble has resembled an occupation neurosis com- 
ing on upon attempts at mastication, cornet-playing, etc. 

Tics occur in the muscles of the trunk and of the extremities, but 
they are rare. Other forms of spasm such as occupation neurosis, re- 
flex, organic and symptomatic spasms, are often enough seen and 
must be clearly separated, both on account of the prognosis and the 
treatment. The causes of the spasms here that are not of the nature 
of true tics are innumerable and consist of trauma, local irritations, 
overexertion, varicose veins, and intoxications. Neurasthenia, hys- 
teria, epilepsy, chorea, writer's cramp and other neuroses may be pres- 
ent as a rule. Spasms of the trunk and limbs therefore are not un- 
favorable from the viewpoint of cure, for they are so seldom essential 
tics. 

Respiratory ties are various, always troublesome and sometimes 
very serious. Singultus, or hiccough, may be of this nature, and may 
or may not prove fatal. Tt is usually a mere reflex trouble, however, 
short in duration" and not alarming. The diaphragm and its innerva- 
tion is of course the seat of the phenomenon. Yawning and sneezing 
are scarcely ever of such a character as to be regarded in the lisrht of 



THE NEURONIC DISEASES 



2t>7 



disease. I recently treated a young man, with a syphilitic history, who 
suddenly began to have uncontrollable yawning spells that so alarmed 
him as to drive him to seek medical advice. Neurasthenic, hysteric, 
•epileptic individuals and those with organic brain trouble, meningitis, 
cerebellar abscess have been troubled with abnormal yawning. As an 
aura of epilepsy it also occurs. A snoring spasm of psychic origin has 
been recorded. A cough that is not of reflex or inflammatory orig-in 
is apt to be hysterical. 

Counter-irritation, internal sedatives and electrization of the 
phrenic nerve are the chief measures that we possess for combating 
these respiratory spasms. Fortunately they are rarely prolonged or 
serious. 

Closely related to the localized tics, if it really be not one of them, 
is the form of torticollis known as spasmodic zvryneck. This is not 
the same as congenital torticollis with its shortening of the sterno- 
cleido-mastoid muscles due to obstetrical injury or prenatal atrophy; 
nor as symptomatic wryneck with its rheumatic, inflamed muscle, tu- 
mors, abscesses, syphilitic lesions and other easily discovered causes ; 
nor as spurious wryneck due to mild caries of the spine. 

Spasmodic Torticollis is a central neurosis and is associated with 
the hysterical, neurasthenic and generally psychopathic constitution. 
The muscles supplied by the spinal accessory nerve are the ones usu- 
ally, or at least prominently involved. Other muscles, however, and 
other nerves are likely to be implicated. Heredity exists in most of 
the cases though it is rarely direct. It involves more especially a neuo- 
pathic taint. Women are much more subject to the trouble than men. 
It occurs in the middle period of life and often follows traumata of 
various sorts, extreme emotional excitement and sometimes no appa- 
rent exciting cause. Stigmata of degeneracy are sometimes seen. 

The disease is a central neurosis of the medulla, more probably 
of the representative centers for the neck muscles in the cortex. It 
is a degenerative trouble and resembles an occupation neurosis in being 
a defect in the coordinating mechanism for the movements of the 
neck. In this form of the disease the spasm is generally of the clonic 
type, tonic spasms being more characteristic of the other forms of 
torticollis. Irregular impulses are sent out from the degenerating and 
defective centers which cause the muscles supplied by particular nerves 
to undergo irregular and intermittent contractions. 

The stemo-cleido-mastoid muscle is the leading one to be involved, 
Dut others are very often implicated with it. The combinations thus 
effected are quite numerous. Some of them have received special 
names because they lead to special movements and attitudes. The most 
common combination is that of the sterno-mastoid and trapezius mus- 
cles. The splenius, scaleni and deep cervical muscles, platysma and 
omohyoid all may be affected. 

In its course the disease passes from one muscle to another. 

In the early days when this disease was not differentiated sharply 
from other forms of torticollis, especially the congenital form, tenotomy 
would be done on one muscle after another as they contracted after 
-each operation. 



268 THE NEURONIC DISEASES 

The attitude of the head and shoulders will of course depend upon, 
the location of the spasm. When only one sterno-mastoid muscle is 
affected the face is turned towards the other side, the mastoid drawn 
down and the chin elevated. Contraction of the trapezius, usually 
the upper part only, which is supplied by the accessorius, causes the 
head to be rotated towards the side of the muscles affected and drawn 
strongly backwards. An alternation of contractions between the sterno- 
mastoid and trapezius muscles causes a sort of circular movement of 
the head that is very characteristic. Other movements are produced 
when other muscles such as the complexus, superior, oblique and 
splenitis are implicated. In most cases the inferior oblique, recti capitis 
postici, major and minor, are included and show involvement of the 
upper cervical nerves. Less frequently the contraction is bilateral. 

Retro-collic spasm is a drawing of the head directly backwards 
by the two trapezii. It is a rare condition. 

Spasmus nutans, salaam spasms, epilepsia nutans, the nodding 
spasm of children, is occasionally a neurosis of the eleventh nerve 
though it is more often a dentition reflex or due to digestive disorder, 
basal meningitis and gross brain disease. It may be associated in 
such cases with transient loss of consciousness and thus resemble or 
be accompanied by true epilepsy. Often it is a mere habit and is a 
veritable tic. It is revealed in a rhythmical nodding or oscillating of 
the head of various degrees of rapidity, even up to fifty and sixty 
times a minute. The eye and facial muscles often participate in the 
salaam. Nystagmus, strabismus and blepharospasm may thus be a part 
of the symptom-complexus. 

In time the muscles undergo hypertrophy in some cases. An 
atrophy of the opposite muscles, as observed by some, is probably due- 
to neuritis or other gross damage. The same may be said of the- 
pain that is occasionally present. A genuine tic does not have pain 
with it but the muscles may feel sore and ache. The spasms as a rule 
cease during sleep and are increased by mental excitement and fatigue. 
They are clonic and recur every few minutes so that it is impossible- 
to keep the head still long. In typical cases there are no objective 
signs of organic, motor or sensory changes. The psychic accompani- 
ments of the trouble occasionally include mental confusion, delirium 
and melancholia. 

The diagnosis calls for a sharp differentiation of spasmodic tor- 
ticollis from the other forms. The shortness of the sterno-cleido- 
mastoid and the fixity of the deformity indicates congenital torticollis. 
Tain, fever, local tenderness belong to the rheumatic type of the dis- 
ease. The usual signs of caries of the spines will aid in excluding the- 
spurious type. All forms of torticollis should, however, be most min- 
utely examined for possible reflex, traumatic, inflammatory or other 
source of the spasm. They must be excluded, of course, before a diag- 
nosis of spasmodic wryneck is permissible. General tic and paramyo- 
clonus may first appear as torticollis. Facial tic, echolalia, define the 
former, whereas associated spasm of the great trunk muscles, bilateral 
in distribution, is the determining feature of the latter. There is noth- 
ing choreic aboul torticollis and if choreic symptoms are present, the 



THE NEURONIC DISEASES 269 

patient has the two affections simultaneously, just as he may have tor- 
ticollis with hysteria, epilepsy and other psychoneuroses. 

The prognosis and treatment follow the lines of that of all the 
tics. I would reiterate and urge especially again here that a most 
careful diagnosis be made to eliminate all possibility of the disease be- 
ing of any of the other forms than the spasmodic. When this is de- 
cided upon, only quiet and rest, sedatives and psychotherapy will do 
any good. I have, like most of my confreres, fallen into the error of 
recommending operative procedures but I have learned not to do so 
any more. The spasm invariably returned, though in some cases there 
was a grateful period of rest. I have seen it immediately reappear 
in other muscles. I have not been so unfortunate as to have seen any 
case made worse by operation, though such observations have been 
made. 

Electricity does no good except for its psvchic influence. Re- 
lapses follow it and cause disappointment and mental depression, 
which are bad for the neurosis. Apparatuses to hold the head fixed aie 
a mere useless torture. General tonic treatment, change of climate, 
change of mental stimulation, change of general regime and environ- 
ment with such occasional sedation as bromides and opiates can give, 
are as effective as any measures we can institute. The cures some- 
times reported as the result of operative and other mechanical meas- 
ures are doubtful because the disease itself is subject to remissions, 
and because most of such cases have not been observed long enough 
after the reported recovery. 

Of course the therapeutic story is an entirely different one for 
the other forms of torticollis. Tenotomy is the thing to do in con- 
genital torticollis. Antirheumatics, antiphlogistics, counter-irritants and 
later on electricity, massage, gymnastics, fixation apparatuses, 
setons, nerve stretching and nerve resection are all to be employed and 
with a legitimate hope of success. Here as elsewhere essential pri- 
mary neuronic degenerative troubles are beyond the power of medicine 
■except so far as the latter can influence their nutrition. The extra- 
neuronic troubles that irritate and damage the neurones secondarily 
•are amenable to treatment — all except the damage to the neurones. 

The discussion of the other forms of torticollis will be found un- 
der the head of diseases of the special nerves (accessorius) in another 
part of the book. 

GENERAL TIC. TIC IMPULSIF. 

This is a remarkable psychonenrosis originally described by 
Guinon and Gilles de la Tourette and often known as the latter's dis- 
ease. Other names that have been given to it are maladie des tics con- 
vulsifs, maladie des tics impulsifs, myospasia impulsiva. Gray sug- 
gested the name palmus. Though the disease is confused by some with 
chorea it is really a psychoneurosis more nearly related to hysteria 
than to anything else. Its spasmodic exhibitions and their inherent 
neuronic origin make the discussion of the trouble in place here. 
When Gilles de la Tourette first described the affection in [885, he 



27O THE NEURONIC DISEASES 

stated that first there appeared a motor incoordination which does not 
affect the general health at all but involves the face and upper extremi- 
ties gradually, the latter usually one-sidedly. Winking, drawing of 
the buccal commissures upward and outward, contraction of the mas- 
seters with grating of the teeth, projection and occasional laceration, 
of the tongue are some of the facial manifestations. The neck muscles 
become involved and there is alternate flexion and extension of the head 
with sometimes inclination to one side or the other by the sterno- 
mastoid spasm. In the upper extremities the fingers are flexed and 
extended and the shoulders raised and dropped. Soon the lower limbs 
participate in the extraordinary performance. In them the incoordi- 
nation is more extensive and involves larger masses of muscular tissue. 
It is unilateral or bilateral. The foot is stamped on the ground or 
the patient stoops over and suddenly becomes erect, or jumps off 
of the floor. The movements are all sudden, rapid and serial. During" 
these strange, violent antics, the inarticulate cry, like the sounds "hem" 
and "ah," occurs and is frequently repeated. Sometimes the sound 
is articulate and loud and resembles some particular word in each 
patient's case. Being repeated echo-like, the symptom has been termed 
echolalia. Oaths, obscene and profane epithets are often emitted,. 
coprolalia, a characteristic which Gilles de la Tourette thought was 
pathognomonic. Sometimes a gesture made to or before him will 
be imitated by the patient, a symptom denominated echokinesis; or he 
will suddenly and involuntarily give voice to some of his most secret 
thoughts, tic de pensee. 

Involuntary, irregular, violent incoordinated movements of par- 
ticular parts of the body, or of the whole of the body, explosive utter- 
ances, and obsessions or fixed ideas constitute the clinical complexus 
of Gilles de la Tourette's disease. 

It is believed that the French authors had their attention drawn 
to this singular hysterical trouble by the publication of Beard in 1880 
upon "The Jumpers of Maine," and of Hammond upon the "Miryachit" 
or Meriatschenje of Siberia and Kamchatka. The Malayan 
Latah is the same thing, as no doubt is the saltatory spasm of Bam- 
berger, mentioned under hysteria. 

There is a neuropathic taint behind this general tic and it is most 
often seen in children between the ages of seven and fifteen. In rare 
instances the heredity has been direct. An outburst of emotion, a 
trauma or an infectious fever has been in some cases the starting point 
of the manifestation. Being a hysterical condition the patients are 
aware of their condition but they cannot help it. In fact they gladly 
yield to it to get rid of the irresistible impulse. It is a lifelong affliction 
as a rule though not absolutely incurable. Remissions occur fre- 
quently. 

The affection must be differentiated from localized spasmodic tic. 
from chorea, from hysterical spasms and paramyoclonus. A careful 
consideration of its complete symptomatology will make the differen- 
tial diagnosis easy. 

Medicinal treatment, as might be expected, proves to be futile. 
Chloroform inhalations, bromides, chloral, mav be useful during the 



THE NEURONIC DISEASES 27 1 

attack to secure temporary respite. The same general treatment used 
for hysteria, with complete isolation as a prominent feature in it, is to 
be adopted here. 

PARAMYOCLONUS MULTIPLEX. 

This is a rare affection, first described by Friedreich. He gave it 
the above name. It has since been called, however, by various names, 
such as myoclonia or myoclonus multiplex, polyclonia, convulsive 
tremor, myospasia. It is characterized by bilateral clonic spasms 
which involve whole muscles or groups of muscles that belong en- 
tirely to the trunk, or are partly attached to it. We know so little 
about the disease that it is difficult to give it a positive classification. 
Not all of the cases that have been described as paramyoclonus multi- 
plex have corresponded exactly with the clinical picture presented* by 
Friedreich's case. This was a phthisical man, 50 years of age, who 
two weeks after a fright felt a stiffness in his body and developed a 
clonic spasm, ten to fifty a minute, in rhe upper arm muscles and mus- 
cles of the thigh, especially the quadriceps. The spasms were bilat- 
eral, were lessened by voluntary movements, occasionally ceased for 
a quarter of an hour and were absent during sleep. Reflex action and 
myotatic irritability were both increased. Galvanic electricity banished 
the spasm for a time but it soon returned. There were no findings in 
the muscles or the spinal cord. Since Friedreich presented and 
named this case others have been described that are extremely sug- 
gestive of tic, of hysteria and of electric chorea. As has well been 
said the moment we diverge from the clinical picture outlined by Fried- 
reich we get close resemblances to other neuroses. Because some 
writers have freely admitted other phenomena under the name para- 
myoclonus multiplex we find it extremely difficult to know just where 
to place the disease. 

Etiology. — Men are more often the victims of the trouble than 
women. It occurs chiefly in adults. A slight hereditary and familial 
influence seems to have been behind some cases. Weiss noted the trou- 
ble in four generations, Gucci in three generations. Its association 
with hysteria, neurasthenia, epilepsy and other familial neuropathic 
tendencies has often been commented upon. It has followed fright, ex- 
treme emotion, severe strain, traumata and infectious disease. 

Pathology and Pathogenesis. — We know 01 no pathological 
changes. The disease seems to be a violent spinal neurosis of some 
sort. Further than this we cannot go, and even this is but a tenta- 
tive statement. There are probably different types of the trouble or 
it may be but a symptom, variously modified, of other well-known dis- 
eases. It is certainly difficult to give the disease a perfect nosological 
independence. Mobius and Strumpell have doubted the independence 
of Friedreich's own form of the trouble. The former identifies it with 
chronic chorea, but his views are not generally accepted. Raymond 
groups it with electric chorea, with which Oppenheim identifies it. 
Others believe that it is merely a form of hysteria though it is usually 
wanting in the sensory, but has revealed seme of the psychic, stigmata 
of hysteria. 



2"J2 



THE NEURONIC DISEASES 



Symptoms. — Here again we meet with a confusing diversity of 
opinion. Just what symptoms should be included under the name 
of paramyoclonus multiplex has not yet been entirely agreed upon. 
There is no dispute about the location of the spasm bilaterally in the 
muscles of the trunk or those that connect the trunk with the limbs. 
It is not accepted that the symptoms can be limited to the limbs. The 
spasm may begin on one side of the trunk, or it may be more marked 
on one side but its bilaterality is one of its chief characteristics. The 
spasms are clonic and may be violent, sharp lightning-like, throwing 
the patient of! his chair and flexing and extending the body, or they 
may be so fine, delicate and tremor-like that they scarcely move the 
part. They rarely are se<m in the face. The limbs have been affected 
with the trunk. The movements may vary from thirty to a hundred 
a minute. They are unsystematized, are symmetrical on both sides 
of the body, are scattered or localized, and are arrhythmical. Single 
muscles or groups of muscles may be involved. Voluntary movements 
repress the spasm, whereas excitement and emotion increases it. They 
are absent in sleep. The withdrawal of the attention causes them to 
diminish. The motor phenomena practically completes the picture. 
The reflexes may be a little exaggerated but there are no electrical 
changes, no mechanical increase of irritability, no sensory symptoms, 
no paralyses, atrophies or disturbance of general nutrition. There are 
no mental symptoms but the patients have often shown an extreme 
susceptibility to suggestion. 

Diagnosis. — The bilateral, clonic, unsystematized spasm, attack- 
ing only the trunk and muscles distinguishes this disease. It has some 
hysterical resemblances but the spasm is entirely apart from the will, 
the muscles involved are not those concerned especially in the produc- 
tion of mental purposive acts and there are no sensory stigmata. Con- 
vulsive tic is possibly somewhat more of an hereditary neuropathy. 
Chorea is less localized and has a somewhat different etiology. Never- 
theless it must be frankly admitted that no sharp lines of differen- 
tiation divide these various neuroses. We may still have to do what 
Raymond has done, group paramyoclonus multiplex with electric 
chorea, fibrillary tremors, non-painful tic of the face and general con- 
vulsive tic, name the group the myoclonias and regard them merely as 
a set of degenerate manifestations. 

Prognosis. — This is grave. The disease has not been cured 
except in very doubtful cases. It may run on for months or years 
and be accompanied by relapses. 

Treatment. — The bromides, chloral and other sedatives, with 
tonics, are available. Galvanism is worthy of a trial. Atropine, hyos- 
cine, and arsenic have been recommended. Hydrotherapy may prove 
useful both as tonic and sedative. 

( KTUPATION NEUROSES. 



By the term occupation neurosis is meant a nervous trouble brought 
v>n by a monotonous, excessive or faulty manner of using the muscles 
concerned in certain special, complicated and coordinated movements 



THE NEURONIC DISEASES 273 

and shown by the inability to perform these movements without the 
loss of other movements involving the same muscles. If the use of 
the adjective functional be applicable at all to disease, it certainly is ap- 
plicable to this disease above all others. An occupation neurosis is not 
only functional in origin, but is apparently itself nothing but a disturbed 
function. It must not be imagined that every sort of inability to per- 
form muscular movements that are caused by occupations are to be 
classified under the head of this neurosis. Many lines of work involv- 
ing cramped positions, pressure upon particular muscles and nerves, 
intoxication as with lead, or direct traumata may set up a neuritis or 
other pathological condition that will decidedly interfere with coor- 
dinated movements. These are not instances of the disease now under 
consideration. This is shown in various ways, but in none more em- 
phatically than in the fact that the prognosis of such is relatively fav- 
orable, whereas the prognosis of the occupation neurosis is decidedly 
unfavorable. 

As the disease occurs in connection with a great number and 
variety of occupations chiefly engaging the hands, a large number of 
names have been given to it. Writing seems to provoke it more than 
anything else and it has more particularly been studied since the intro- 
duction of the use of the steel pen in the early part of the last cen- 
tury. It is commonly called therefore writer's cramp, or scrivener's 
palsy. Occupation spasm, fatigue neurosis, coordinated occupation 
neurosis, professional neurosis are some of its synonyms. An inter- 
minable list of names for it 'is made up of those describing the partic- 
ular form of occupation in which it occurs, as for example, pianist's 
cramp, telegrapher's cramp, milker's spasm, sewing spasm, etc. Writ- 
er's cramp, graphospasm, mogigraphia, in a word, so-called occupa- 
tion neurosis, is a distinct disease, and should always be carefully differ- 
entiated from other conditions that may at times closely resemble it. 

Etiology. — The etiology has some remarkable features about it 
that are extremely suggestive. A neuropathic constitution and a par- 
ticular occupation strain cover the main points in regard to its causa- 
tion. The disease is rarely seen in one who inherits a perfect nervous 
constitution. In some cases there is a distinct nervous heredity, actual 
disease having appeared in the immediate ancestry ; in most of the 
cases there is merely a transmission of a neuropathic predisposition. 
I have never seen a case in which I could not trace this neuropathic 
inheritance more or less distinctly. Neurasthenia, hemicrania, epilepsy, 
neuralgia, convulsive tic, phobia, and tabes have been seen and recorded 
in association with it. Worry and intemperance that are said to predis- 
pose to it may be but a revelation of the same neuropathic basis upon 
which it likewise rests. The artistic temperament is generally neu- 
rotic, and this neurosis occurs frequently among artists when they 
overwork their muscles upon musical instruments. Several members 
of the same family have been stricken with the trouble. 

The influence of a nervous temperament cannot be doubted. Men 
are more frequently affected than women probably because the}- are 
more exposed to the overexertion, by reason of business life that 
brings it on. They suffer especially from the motor form of the trou- 



274 



I HE NEURONIC DISEASES 



ble. It occurs at all ages, though by far the majority of cases are seen 
between the years of twenty and forty. 

That there is something behind the disease of a constitutional 
nature that provokes it in addition to the mere overuse of the muscles 
is shown by the remarkable fact that in some occupations wherein 
women predominate, the men are still the greater sufferers. For ex- 
ample, Lewis has found that in this country telegrapher's cramp was 
seen in only four women out of forty-three cases, though women are 
employed in telegraphing in a much larger proportion to men than 
these figures would represent. 

The exciting cause of the disease is the overuse of a particular set 
of muscles. This is perhaps not a perfectly accurate way of stating 
it. As these same muscles respond to the will in other forms of move- 
ment than that which brought the trouble on, it should be stated that 
an excessive, monotonous employment of a particular form of com- 
plicated, coordinated movement causes it. This presents the affection 
in an entirely different light and begins to let some illumination in upon 
its manifest connection with a neuropathic temperament. It is the 
overuse of a movement, and not merely of the muscles, that underlies 
the trouble. 

Movements are primarily of brain or mind origin, whereas mere 
nerves and individual muscles are represented in the spinal centers. 
This etiological fact that complicated, coordinated movements rather 
than mere nerve or muscle activity is the cause of the occupation neuro- 
sis sharply differentiates this disease from the affections that simulate 
it but depend upon poliomyelitic and neuritic changes. 

Not every kind of movement provokes it, but those painfully and 
slowly acquired, educated movements, that are highly complicated and 
require an extreme degree of a novel form of coordination, that were 
and are purely voluntary, but by practice have grown to be automatic, 
and that bring into play an unwonted, antagonistic set of muscles. In 
writing, playing musical instruments, milking, beating a drum, manipu- 
lating a telegraphic key, there are several combined acts being per- 
formed at the same time and under the same strain. Not only is firm 
prehension exercised by some muscles while others at the same mo- 
ment are performing the required movement, but both are under an 
unusual tension that at first consciously and later unconsciously gives 
unwonted exercise to the cerebrum and the central coordinating appa- 
ratus. In writing, for instance, the pen must be held more or less 
firmly and it must be properly moved by both fingers and the arm. 
This is a compound, complicated act therefore. It means a remark- 
ably sharp disassociation of the movements of different sets of mus- 
cles all in the same extremity and at the same period of time. This 
requires an extraordinary adjustment of function between different 

of motor centers in the cord and brain. It opens up new path- 
ways of inter-communication between these centers and by the nature 
of the process puts these new pathways, and with them the new coor- 
dinating apparatus, into a condition of severe strain. Exhaustion takes 
place and though the associated motor centers may operate and cause 
the muscles to contract in other ways and along other coordinating 



THE NEURONIC DISEASES 275 

paths, they cannot do so along these that have become thus wearied. 

That the mere overuse of the muscles alone is not the cause of 
the trouble is shown in the fact that neither authors nor stenographers 
who write a very great deal are victims to any great extent. Copyists 
and those who use a cramped hand in writing and pens that prevent 
a free movement of the arm are the great sufferers. Resting the hand 
on the little finger and moving the pen up and down with the other 
fingers while the arm remains comparatively quiet and poised seems 
to be a particularly dangerous method. Sharp steel pens require so 
much more stiffness and firmness in movement than do soft, loose 
quills that they have been in fact justly blamed for the trouble. The 
style of writing, the intensity of it caused by hurry to get through, the 
instrument employed and in fact everything that increases the demand 
upon the coordinating apparatus are etiological factors. To this must 
be added, of course, the monotonous exercise. 

What is said of writing applies with equal force to all other occu- 
pation movements from which the disease has developed. In the irreg- 
ular yet carefully regulated movements of the telegraphing arm and 
hand, we observe a strained coordination of a highly complicated 
character. The pianist, the violinist, the flute-player, the milker, the 
drummer, the cigar-roller, the seamstress, the tailor, the cobbler, the 
dancer and others are usually employed in an occupation that upon the 
face of it shows an unusually fine coordination between various com- 
bined and antagonistic groups of muscles. At first this coordination 
was practiced with difficulty. It had to be learned. It tends to become 
automatic, but has not yet reached the degree of complete automatism. 
It is subject to weariness and to depression if the guiding cerebral 
centers are vitiated by heredity and other predisposing factors. Mo- 
notonous and excessive exercise of it breaks it down. 

Local inflammatory conditions in the hand, injury, wet and cold, 
albuminuria, lead-poisoning and other causes of neuritic degenerative 
conditions have been blamed for it, though it is a question whether 
these cases should be regarded as typical instances of the disease. I 
am sure some of the latter are but cases of neuritic incoordination, 
spasm or palsy and are no more to be regarded as cases of occupation 
neurosis than the ataxia of tabes is to be regarded as the same as psy- 
chic vertigo. 

Emotion is an etiological factor. 

I ' athology and Pathogenesis. — No pathological changes have 
been found in the few cases that have been examined post-mortem. It 
will not do, however, to say with Oppenheim that none will probably 
ever be found and it is entirely a misconception of the disease to attrib- 
ute it to the neuritis and poliomyelitis evidenced in some supposed 
cases of the disease that were examined pathologically. It is undoubt- 
edly a functional trouble, but functional troubles must necessarily 
spring out of some minute nutritional changes, albeit the latter are 
too fine for our modern means of investigation. Consider for a moment 
the etiology of this strange disease. Note how a tendency, a neuro- 
pathic tendency, born in the individual or fostered by his environment, 
plays a leading role among its predisposing causes. Note the diseases 



276 THE NEURONIC DISEASES 

with which it has been associated; neurasthenia, functional spasm, epi- 
lepsy, hemicrania, hay fever, neuralgia, chorea and a tendency to want 
of all self-restraint, sobriety and regularity that go with a strong 
and healthy mentality. Observe its frequent association with emotional 
states, with wasting diseases, depressing traumata and a mode of life 
that is unhygienic in its surroundings and duties. The background 
upon which the disease portrays itself is suggestive indeed and makes 
one think involuntarily of the hysteroid and other mild psychoses and 
subconscious, cerebral exhibitions. 

After considering the etiology of the disease, observe for a mo- 
ment how it reveals itself. It is preeminently a motor trouble. The 
disturbance occurs in a variety of movements that are of late acquisi- 
tion, are educational, are striving to become automatic and are already 
partly so, and are the result of a most complicated and refined form of 
coordination that is too coarse to be wholly cerebral in origin and yet 
not coarse enough to be spinal, but just of such a character to be sub- 
conscious, subpsychic, like some of the phenomena of hysteria, phrenas- 
thcnia and other forms of cerebro'-psychosis of the subconscious order. 
Place this beside the fact that the disease is not essentially neural or 
muscular because other movements can be readily made by the same 
muscles, as witness the disabled telegraph operater writing with great 
ease and fluency ; beside the fact that none of the usual signs of mus- 
cular or neural disease, electrical or otherwise, are observed in typical 
cases ; and finally, besides the fact that the prognosis is bad and the 
treatment discouraging, it seems to me we have enough data to sug- 
gest that the trouble is essentially central in origin, is a subconscious 
cerebration and is a functional weariness or exhaustion of the coordi- 
nating apparatus. 

It is easy to understand of course that the excessive use of the 
muscles which provoke the disease, but which does not represent it in 
its essential nature, for it is not muscle exhaustion so much as it is 
exhaustion of the central inhibitory, coordinating apparatus, may in a 
reflective manner cause atrophic conditions and even occasional fugi- 
tive nenritic and poliomyelitic changes of a slight character. Exhaus- 
tion of functional coordination with certain variable secondary changes 
of a grosser nature constitutes then, so far as logic can demonstrate 
to us in the absence of more positive physical findings, the pathogene- 
sis of the true occupation neurosis. Here again it is shown that this 
disease must not be confounded with the spasmodic pareses that often 
simulate it but that owe their origin to some limited form of muscle 
or nerve disease such as myositis, neuritis, poliomyelitis. 

SYMPTOMS. — The onset of the trouble is always gradual. It is 
first noticed that the use of the hand is becoming uncertain and be- 
yond the delicate control of the will. Not only does the writing 
seem to grow more difficult but it begins to change in character. There 
is a tremulousness about it. a little jerkiness, a disinclination to pro- 
ceed in the old regular way. Sometimes a feeling of soreness or weight 
or slight pain is felt in the fingers, up the arm and between the should- 
der blades. A little writing may still be done normally, but lengthy 



THE NEURONIC DISEASES 277 

use of the pen produces a feeling of extreme tire and a stiffness and 
unnecessary rigidity in holding. 

The symptoms of the fully developed disease are necessarily varied 
because the many occupations in which this neurosis occurs demand 
the use of many different sets of muscles and nerves. There is no 
fixed clinical picture therefore for the neurosis in general though there 
is more or less of a definite manifestation in each special occupation. 
There are, however, three well-recognized types of the trouble, namely, 
the spasmodic, the paralytic and the tremulous. When there is much 
pain present, the type is referred to as neuralgic. So much more prom- 
inent are the motor symptoms that the affection may well be looked 
upon clinically as a motor neurosis. 

In writer's cramp the attempted use of the muscles at once de- 
velops a spasm. They become stiff and seize the pencil and the move- 
ments are awkward and uncontrollable. Sometimes other muscles than 
those merely necessary to perform the act of writing participate in the 
spasm. The left arm has thus exhibited an associated condition. More 
often when the left arm is employed to relieve the affected right, the 
latter immediately becomes spasmodic. More rarely even the legs 
have been seen to be spasmodic when only the writing with the right 
hand provoked the trouble. A hemispasm of the entire body has been 
reported and suggests strikingly the seat of the primary lesion. The 
spasm in the fingers is tonic and affects the muscles concerned with 
the performance of the act. Some authors insist that the latter is an 
essential indication of the disease, but Lewis does not. The flexors of 
the fingers, more rarely the extensors, are contracted. The thumb and 
index finger are especially marked by the spastic weakness. The thumb 
may be controlled and pressed firmly into the palm while the fingers 
are forcibly separated. Sometimes the spasm is so promiscuous and 
spread about that the whole hand seems to be in a state of riotous 
movement. As it begins to appear the patient changes the method of 
holding his pen and thus all sorts of bizarre and even ludicrous posi- 
tions are adopted in order to be able to go on with the writing. Per- 
sistence in the writing even with the new attitude causes the spasm 
to appear in other muscles so that the work has to be given up entirely. 
A condition almost of tetany may develop, with contraction of the flex- 
ors of the wrist as well as of the fingers upon the slightest attempt to 
use the muscles for writing or any other purpose. Mitchell described 
a lock-spasm in which the contraction of the fingers and hand was 
so violent for a time that the latter seemed to be locked. When the 
spasm wears off the muscles relax — feel a little tired and weak. In 
some cases there is during the spasmodic condition severe pain in the 
muscles, bones and joints. A significant fact is that the more the 
patient worries over his inability and the more frantic his efforts are 
to overcome it, the worse the disturbance is both motor and sensory. 

The paralytic form of the disease is less common than the spastic. 
Like the latter it comes on gradually and has other symptoms occa- 
sionally associated with it. The fingers, hand and arm are subject to 
a feeling of intense weariness and when writing is attempted they re- 
main immobile and like a dead weight upon the table. The will seems 



27* 



THE NEURONIC DISEASES 



to have lost all power over them. Sometimes this paresis follows a 
spasm. Paresis in one muscle with spasm in another has been seen. 
Rarely a paralytic condition is followed by a spasmodic. The result 
in regard to the occupation is the same. Inability, awkwardness, with 
strange and frantic efforts to overcome and thwart it are so obvious at 
times that the attitude alone is almost sufficient to make a diagnosis 
upon. In the paralytic form a certain degree of muscular atrophy is 
occasionally noted. It is unlike the wasting of the progressive form of 
atrophy in the fact that it is less in degree and it is amenable to re- 
covery. If it is an early manifestation and is accompanied by local 
pain and paraethesia, neuritis is probably the cause of the trouble and 
not the neurosis under consideration. A mild, localized, permanent, 
late atrophy may rarely occur as the result of secondary damage down 
to the central cells of the cord by the severity and prolongation of the 
neurosis. None of the usual objective signs can be elicited by exam- 
ination. When electrical reactions, cutaneous sensibility, true objec- 
tive paralysis, tremor or ataxia is observed the disease is not one of 
occupation neurosis but some organic trouble of peripheral nerves or 
cord. Too much inportance cannot be given to this distinction, for 
the prognosis and treatment depend upon it. 

It is very rare for patients to complain of tremor and yet in some 
instances an irregular tremulousness has been observed. One must 
be well on his guard not to mistake dementia paralytica or disseminated 
sclerosis, which sometimes in their incipiency reveal only a tremor 
and partial inability to write, for this disease. As an exhaustion mani- 
festation, tremor, or rather trembling or unsteadiness, may well be 
expected, especially in the forefinger when the hand is at rest. An 
unusual form of nystagmus has been seen among miners and attributed 
by Nieden to the defective illumination of the mines causing eye-strain. 

The neuralgic forms of the trouble must be carefully studied in 
a skeptical frame of mind. Authors describe all sorts of painful condi- 
tions that are clearly due to neuritis. One writer speaks of pain over 
the nerve trunks elicited by pressure, of hyperesthesia, anaesthesia and 
paresthesia, all typical of a distinct neuritis. What is the logic of 
having two descriptions thus of the same disease in different parts 
of the lx>ok? If this author regards the occupation neurosis as an 
expression of a neuritis or other pathological change, it can and should 
l>e kept under the symptomatology merely of neuritis; if the occupation 
neurosis is not a distinct disease of such gross organic origin, then 
these symptoms of such organic disease do not belong to it and should 
not be referred to except as an evidence of a complication. Clearness of 
distinction and logical reasoning are in neurology as in every science 
coequal in importance to the mere accumulation of facts and observa- 
tions. Complications and sequelae may he easily understood as ac- 
companying an occupation neurosis. Organic gross changes and in 
9ome advanced cases even undiscoverabk histopathological changes of 
a nutritional character may cause various vasomotor and trophic symp- 
toms. These, as a rule, will represent nenritic and poliomyelitic disease 
which will differentiate the trouble at once from an occupation neurosis. 

Diagnosis. For the sake of clearness we must in this disease 



THE NEURONIC DISEASES 2/9 

maintain a sharp distinction between a functional and an organic 
trouble. It is confusing, unscientific and illogical to talk about a 
neurosis being a functional trouble and distinguished from organic, 
and immediately under the head of neurosis begin depicting the well- 
recognized clinical pictures of distinct organic diseases. And that is 
just what the older writers have done and alas ! what the later writers 
are still doing. Neurology cannot hope to be clear to the general reader 
when its followers thus wantonly jumble its well-known facts. I am 
not criticising the difference of opinion in regard to the real nature 
of the occupation neurosis, for I admit that there is much room for a 
difference of opinion, but I am criticising the method of calling a disease 
one thing, functional, and then describing it with the symptomatology 
of another well-recognized thing, organic. The logical contradiction, 
not the difference of opinion in connection with the disease, is the 
ground for my criticism. 

I have perhaps already sufficiently shown that in my opinion an 
occupation neurosis is not a neuritic or muscular disease itself, though 
as a complication or a sequel it may have accompanying it a neuritic 
or muscular organic trouble. Its etiology and its symptomatology, as 
I have previously shown, both loudly declare that it is a disorder of the 
higher conscious or subconscious coordinating mechanism. Y\ nether 
this mechanism resides in the cortex, basal ganglia, cerebellum, medulla 
or gray matter of the cord we cannot say. But its location is of little 
consequence in comparison with the fact that it is a highly compound, 
complicated function dependent upon the play of one source of nervous 
impulses upon another source. If the sources of these impulses them- 
selves are organically diseased, we may have spasms and pareses with 
incoordination. Such diseases will be recognized as well-known organic 
lesions of the brain, cord or nerves. On the other hand, the mere 
functional play of one source of impulse upon another source, the new, 
educated function as it were, is disturbed and exhausted. This is a 
true occupation neurosis. 

There are many diseases in which muscular weakness and dis- 
turbed coordination with spasm are seen and must be differentiated 
carefully from this disease. Every sort of disorder of writing is not 
writer's cramp. The former is seen in multiple sclerosis, in high tabes, 
in dementia paralytica, in paralysis agitans, in hemiplegia, in chorea, 
in progressive muscular atrophy and various injuries and lesions about 
the hand and related nerves. The differential diagnosis of these is 
easy as a rule and involves always the diagnosis of the organic or 
general trouble. 

The two diseases that have been most confused with writer's cramp 
are neuritis and poliomyelitis. In all these there are motor, sensory 
and other exhibitions that lead at times to a close simulation between 
them. 

Neuritis has very often been mistaken foran occupation neurosisand 
vice versa. A neuritis certainly interferes with complicated movements 
and it may spring from the same general predisposing and exciting 
causes in some instances as an occupation neurosis. The necessity 
for a clear recognition of a distinct difference between the two, how- 



280 THE NEURONIC DISEASES 

ever, is indicated in the opposite character of the. prognosis of the 
two diseases. Neuritis is a local, distinct, comparatively permanent 
lesion with definite, constant symptoms. In neuritis the sensory symp- 
toms are in great evidence often and are always more or less present. 
They certainly hold a much more exalted degree of prominence in re- 
lation to the motor symptoms here than they do to the motor symptoms 
in an occupation neurosis. In the latter we often have muscular, 
crampy pains, general soreness and widely distributed fugitive aches, 
but we don't have the localized pains upon pressure in the nerve trunks, 
the localized spots of hyperesthesia and anaesthesia, the well-defined 
and unmistakable parsesthesise like numbness, tingling, burning, pins- 
and-needles sensation of neuritis. The sensory phenomena of the latter 
are prominently cutaneous and objective ; those of the former are 
largely muscular and subjective. 

Neuritis suggests clearly an organic, well-defined local lesion ; an 
occupation neurosis has a sort of resemblance to neurasthenia or 
hysteria. It is in the motor sphere that the difference between a neuritis 
and an occupation neurosis comes out most clearly. Incoordination, it 
is true, is prominent in both. In the former it is incidental, in the 
latter it is all but the entire disease. There is definite weakness and 
paralysis in individual muscles, so that for no sort of movement can 
the muscles be exercised in neuritis ; in the neurosis there is only ex- 
ceptionally paresis and then only as a result of prolonged and monot- 
onous exertion. In the neurosis the muscles may be powerless to move 
for one sort of movement, but apparently little affected for the per- 
formance of another sort of movement. A victim of pianist's cramp 
may be able to write normally ; an affected telegrapher can still play 
the piano; and one who can no longer write may still be able to draw 
with the greatest facility. When the trouble involves the lower ex- 
tremities other movements than those which caused it can usually be 
well performed. This argues against the old view that the muscles 
themselves are diseased. The electrical changes, so well known in 
neuritis, the reaction of degeneration, are not seen in the neurosis. The 
presence of atrophic, vasomotor and secretory local disturbances, loss 
of the reflexes, pareses and similar manifestations in other parts of 
the body point to a neuritis. Neuritic symptoms are bilateral, when 
they are bilateral at all, from the start. In the neurosis, an attempt to 
use the other arm may set up bilaterally the same trouble in it, but the 
disease is never bilateral from the beginning. 

As I have said, all of these neuritic manifestations may occur in 
the course of an occupation neurosis, but in my opinion they represent 
a complicating neuritis. Tf T thought the disease were entirely a form 
of neuritis, it would be referred to merely as a symptom of this disease 
described elsewhere. The frequent disappearance of the neuritic symp- 
toms while the incoordination and difficulty in writing continue shows 
also that a neuritis and an occupation neurosis are not the same thing. 

PoliomyeliHc symptoms may occur also in the course of an occu- 
pation neurosis, but they are easily differentiated. In poliomyelitis 
there is a febrile condition, a regressive paralysis finally limiting itself, 
al *ng witli rather rapid atrophy in particular muscles. Poliomyelitis 



THE NEURONIC DISEASES 28l 

occurs most frequently in the legs; the neurosis in the arms. Spasm, 
pain and true incoordination are wanting in poliomyelitis. The sore- 
ness of the muscles, the fatigue symptom, the appearance of the in- 
capacity upon the initiation of a particular form of complicated, ac- 
quired movement are also absent from the spinal inflammatory de- 
generative trouble. 

Tetan-v has been mistaken for an occupation neurosis. Tetany 
is provoked by any sort of movement, whereas this disease has its 
spasms initiated only by an attempt to resume the occupation that 
caused it. 

The "hcphccstic hemiplegia''' of Dr. Frank Smith seen among 
Sheffield smiths is declared by Gowers to have been cases of organic 
disease. of the hemisphere. 

Types of the Disease Based upon Occupation. — Practically the 
trouble is always of the same nature in whatever occupation it may 
have been acquired. It is useless therefore to go into any elaborate 
description of all the forms of the disease that have been seen and 
reported. The principal feature of investigation in each particular 
case is the character of the movement that has brought the trouble 
on and the particular muscles involved in the elaboration of that move- 
ment. The whole question is therefore one of location merely and of 
gross anatomy. This investigation will have, however, rather a scien- 
tific interest merely than a therapeutic one, for the treatment is the 
same in all cases. It may be of value diagnostically, however, if the 
occupation can be guessed from the symptoms of the disease alone. 

Pianist's cramp is chiefly a professional disease and seems to 
occur, possibly on that account, more among women than men. The 
spasmodic and neuralgic varieties of the disease, more particularly the 
latter, are seen. Precision in striking the key and prolonged extension 
of the fingers are troublesome manifestations. Pains are often felt in 
the fingers, up the arms, in and about the shoulder and between the 
shoulder blades. Gowers mentions a case that had pain in the outer 
border of each hand, but never any cramp except at night. Playing, 
of course, has to cease as soon as the symptom appears. Paralytic forms 
and others occur, but usually pain and exhaustion during playing repre- 
sent the complexus of symptoms. Violinists may be affected in either 
or in both hands. In flute players the left hand is more often involved 
than the right. In a young cornetist that I once treated who had failed 
to get much improvement from many previous lines of treatment and 
who improved, but I cannot say recovered, after a long course of treat- 
ment with me, the lips were slightly spasmodic and there was an in- 
definite soreness along the course of the supraorbital nerves. He was 
distinctly a neuropath, but exhibited at 110 time any other local symp- 
tom. Aldrich reports a case in a trap-drummer whose duty it was 
to beat a drum by the operation of a pedal manipulated with the right 
foot. Cramping pain and a sense of exhaustion seemed to be located 
in the tibialis anticus and peronei muscles. The symptoms appeared 
only when playing or when walking rapidly. 

I once had at my clinic for a long time what seemed to be a 
clear case of the disease in a painter. The possibility of lead-intoxici- 



282 



THE NEURONIC DISEASES 



tion was eliminated by the absence of the extensor paralysis, the abdo- 
minal colic, the blue line along the teeth and other well-known signs 
of saturnism and lead neuritis. He could move his arms somewhat, 
but there was no spasm and only soreness in them. He had been work- 
ing hard and continuously for a long time on a steady job and told 
me he had scarcely ever rested his right arm by using his left. 

To blacksmiths is known a very painful occupation cramp involv- 
ing especially the deltoid and biceps muscles. Seamstresses, tailors 
and others who do sewing, such as sail-makers, carpet-weavers, suffer 
at times from the disease. Runge believes he has seen it in waiters 
from carrying plates and glasses. Cigarmakers who roll cigars all day 
and milkers of cows have the cramp sometimes. Oppenheim has seen 
it appear in barbers every time they had to use the razor. It was 
spastic in character. Lapidaries are not free from the neurosis. A 
metal-chaser has suffered from it. Among the other numerous trades 
that at rare intervals cause it may be mentioned -Rower-makers, turners, 
watchmakers, knitters, engravers using the burin, masons handling the 
trowel, compositors, cnamelers, shoemakers and money-counters. A 
sawyer's cramp is described by Poore. 

These trade neuroses, so to speak, are not as frequent by any 
means as the neuroses caused by writing, music playing and telegraph- 
ing. 

Telegrapher's cramp seems to affect more particularly those who 
use the Morse system, which necessitates an up and down movement 
of the key. The typewriter may produce the trouble just as piano- 
playing does. 

Stammering and stuttering from much speaking is related to this 
disease, so is the painful exhaustion of the laryngeal muscles called 
mogiphonia by Frankel. 

A dancer's cramp is known among ballet dancers. 

It would seem that every form of human occupation, involving 
strained, continuous and complicated, coordinated movements is liable 
to provoke this neurosis. Still the caution must be repeated not to con- 
found neuritis with its degenerative symptoms and which lurks behind 
the occupation palsies with this neurosis. 

Prognosis. — Some authors affirm that the prognosis of writer's 
cramp is variable. It is if the symptom alone is made the disease. 
If the trouble is confounded with a neuritis the prognosis naturally will 
be favorable, for that is the prognosis of neuritis. Of the disease occu- 
pation neurosis, as I conceive it and have endeavored to describe it, 
the prognosis is decidedly unfavorable. It runs parallel with the sort of 
prognoses that we have to make in hysteria, neurasthenia and allied 
general disorders. Amelioration occurs after periods of prolonged rest. 
Absolute cures have been seen, but they are rare. As a 
rule the disease continues many years or for life, relapsing or 
rather breaking out in a sort of exacerbation every time the original 
movements that caused it are attempted. There is danger always in 
using the other hand, as writers and telegraphers so often do, for it 
frequently also becomes affected. Tt never destroys life. 

Treatment. — Prophylactic treatment is of great moment. The 



THE NEURONIC DISEASES 283 

instant the first premonitions of the trouble appear cessation of the 
occupation must take place. All writing had better be given up for a 
time. The prophylaxis is summed up in the ore phrase, avoid all stiff, 
cramped, uncomfortable attitudes, style of writing and manner of hold- 
ing the pen. Place the body at the desk in writing so that an easy, 
loose and pliable position can be maintained. Adopt a style of writ- 
ing that is large, full, round and flowing. Use soft pens in thick 
•cork handles. It is good to vary the attitude and the penholder from 
time to time. Whether writing or telegraphing the entire arm should 
rest on the table. The vertical style of penmanship is said to be less 
liable to produce the trouble than is the slanting. Each case is to be 
studied from its own standpoint, but ease of attitude, ease of mind, 
largeness of movement and frequent relaxation, are among the im- 
portant preventive measures to be remembered. The rest should be 
absolute and not merely a variation of exercise. It is unwise to go 
from much writing, for instance, immediately to piano-playing. The 
two neuroses have been seen to develop thus simultaneously in the 
same individual. 

When the trouble has fully declared itself, only absolute and pro- 
longed rest is the safe plan to adopt. Those who must write some at 
all hazards may be guarded somewhat by the use of a special apparatus 
to hold the pen with. These are very numerous and consist of rings 
and bracelets for several fingers, in which the penholder can be fastened. 
The attitude of the hand is decidedly altered while the writing goes on. 
All instrument makers have several forms of apparatus of this sort," 
specially commendable among them being the Matthieu finger ring 
and thumb rest, the Nussbaum finger bracelet and others. 

There is no drug treatment for this neurosis. Of course the 
neurasthenic state may call for its special tonics. The very nature of 
the disease, an exhaustion of coordination, precludes any hope of benefit 
from mere medicinal agents. 

Electric treatment is also ruled out by the nature of the disease. 
Galvanism has been applied to the cervical cord in some cases with 
alleged benefit. As everyone knows electricity is a most valuable agent 
in the treatment of the degenerative neuritic troubles, both galvanism 
and faradism. It is to be noted, however, that those who claim such 
excellent results from the electric treatment of writer's cramp do not 
distinguish sharply between the pure functional occupation neuroses 
and the neuritic professional palsies. It is easy to understand therefore 
how even their results vary so extremely. 

Massage and gymnastics afford the best results. The former 
maintains the nutrition while the muscles and nerve centers are regain- 
ing their tone from rest, and the latter changes yet engages the activities 
of the central coordinating apparatus. Swedish movements of the 
hands and fingers with resistance on the part of the patient are particu- 
larly good. The fingers and wrist are flexed and extended, adducted 
and abducted. The pressure must be regular, the seances short and 
the practice several times a day. Gentleness, persistency and the end 
to be attained, the restoration of wearied muscles and exhausted co- 
ordination, are to be kept clearly in mind. 



284 THE NEURONIC DISEASES 

Suggestion and psychic treatment has some influence, as psychosis 
enters to a certain extent in the loss of the coordinating power. 

Tenotomy and nerve-stretching are mentioned merely to provoke 
the wonder why they were ever thought of. 

MYOTONIA CONGENITA. 

This singular affection is sometimes called Thomsen's disease,, 
because this physician, who was a victim of it, and in whose family 
there were more than twenty cases in five generations, gave the first 
complete and accurate description of it. Before him Sir Charles Bell, 
Benedict and Leyden had each referred to it. Since the prominence 
which Thomsen conferred upon the disease it has been quite closely 
studied by Seeligmuller, Westphal, Mobius, Erb, Striimpell, Yig- 
ouroux, Hammond, Dana, Shaw and many others. It is not a common 
disease, though upwards of half a hundred cases perhaps have been 
reported. It is more frequently observed in Germany and Scandinavia 
than in England, France or America. Its exact position in the classifi- 
cation of diseases cannot be determined for reasons- noted in the dis- 
cussion of its pathogenesis. 

Etiology. — The predominant feature in its etiology is its heredity 
and occurrence in the same family. A few isolated cases have been 
observed in which the hereditary influence has been chiefly neuropathic. 
Males are said to be more frequently affected with it than females. 
The disease may appear in early childhood about the period of 
adolescence. It is not known to be dependent upon any exciting causes 
for its outbreak, though as it appears to be an expression of defective 
development, all depressing and exhausting surroundings may have 
something to do with hastening its appearance. 

Pathology and Pathogenesis. — So few cases have come to 
autopsy that our knowledge in regard to the essential basis of the 
trouble is far from being adequate. In the cases of Erb and others 
there was hypertrophy of the muscular fibers, increase of the sar- 
colemma nuclei and an overgrowth of interstitial tissue. The fibers 
have been reported as being diminished in size, though increased in 
number. All of the muscles, even the diaphragm, have exhibited this 
change. Dejerine and Sottas have confirmed these findings and added 
the statement that in their case the brain, cord and nerves were entirely 
normal. In some cases absolutely no changes have been observed either 
in the muscular or the nervous tissues. 

The symptoms of the disease, taken in conjunction with these 
almost negative pathological findings, favor the hypothesis that it is 
a functional trouble. Most writers following Leyden have described 
it .is a functional disease o\ the muscles, not including it at all under 
tin- head of nervous diseases. This is extraordinary in view of the 
neurotic and psychic relationships of the disease. And yet it is but 
fair to state that these authors look upon the mental deterioration and 
tin- nervous manifestations and influences often observed in the dis- 
ease :is of the nature of mere complications, The same developmental 



THE NEURONIC DISEASES 285 

inadequacy that affects the muscular apparatus affects the nervous cen- 
ters. 

Other authorities classify the disease with the dystrophies, not 
merely because there is a certain similarity in some of the clinical fea- 
tures with the latter, but because they suspect that it, as well as the 
d}Strophies, are remotely dependent upon some minute central change 
in the central nervous apparatus, which may ultimately show that the> 
are closely related to the central progressive muscular atrophies. 

A third group ot writers are inclined, to regard the trouble as 
hysteroid in origin, though not in any sense hysterical. They explain 
that it is a sort of psychosis, a psychic incoordination, a connecting 
link between mental and bodily ailments. 

The absence of constant and distinctive pathological findings fa- 
vors the functional character of the disease. The hereditary and de- 
velopmental origin of the disease, its chief limitation to the voluntary 
muscles, its close relationship to the volitional faculty, the frequent 
mental defectiveness and the absence of most of the well-known signs 
of typical organic disease of the brain or spinal cord lend some sup- 
port to the mental theory. 

With the meagre data now at hand nothing definite therefore can 
be said in regard to the pathogenesis of this remarkable affection. 

Symptoms. — The prime symptom of Thomsen's disease is an 
intentional spasticity. I use the adjective intentional here in the same 
sense in which it is used when the intentional tremor of multiple sclero- 
sis is spoken of. 

In the muscles of the extremities and of the face the slightest voli- 
tional movement causes a slow, firm, irresistible contraction. This may 
occur at any time when the patient starts to use the particular muscle or 
set of muscles. It is usually, however, most prompt and severe after a 
period of rest. With a powerful exertion of the will the contraction 
can be retarded and even at times overcome. Thus it is seen to be a 
volitional phenomenon in part, albeit a markedly abnormal one. 

Some have endeavored to explain the entire disease on this per- 
version of the volitional muscular function. It is argued that to pro- 
duce a. desired movement the volitional faculty, so-called, must exer- 
cise a combined, normal control over every muscle of the body and its 
antagonist. It must preserve a balance between the two. If this 
balance is lost, the muscles do not work well together, action and over- 
action causes an unnecessary expenditure of force, and a sort of pur- 
poseless movement. As one author has put it, an inhibition of volun- 
tary movements due to a muscular rigidity sets in during the action. 
Influences like increased emotion that affect the will affect most strik- 
ingly the contractions. Often when the contraction initiated by the 
will is once started it cannot be stopped, even with the greatest exertion. 
After several such tonic contractions they become gradually weaker 
and finally cease altogether from exhaustion. They do not reappear 
until another voluntary movement is instituted in them. 

Warmth, mental quietude, non-observation of self, frequent exer- 
cise of the involved muscles and ingestion of a small amount of alcohol 
will tend to diminish the severitv of the contractions. 



286 



THE NEURONIC DISEASES 



All the muscles of the body except the viscera and involuntary 
muscles may be the victims of the disease. Swallowing, therefore,. 
may be difficult. Speech is affected. Protrusion of the tongue may 
cause it to be caught and bitten between the teeth. In grasping an 
object the hand closes like a vise. The act of walking becomes stiff > 
sluggish and irregular. The patient may even fall and remain rigid. 
The ocular and laryngeal muscles, with the sphincters, escape. 

In repose the muscles are normal to the touch ; in contraction they 
arc hard and firm. They may be normal in size or slightly enlarged 
or diminished. Sometimes their contour is abnormal from implication 
of a part of a muscle group. There are no disturbances of the re- 
flexes. 

In Erb's so-called myotonic electrical reaction in the muscles cer- 
tain changes take place in the responses to the galvanic current, those 
to the faradic remaining normal. There is a muscular contraction 
of long duration. The muscles show an increased excitability to the 
direct galvanic current. Only contractions upon closure are obtained. 
Anodal closing contraction is usually the more marked. This is 
somewhat of a reversal of the normal phenomena. With a stabile 
galvanic current a vermicular, rhythmical, wave-like contraction passes 
through the muscle from the negative to the positive pole. 

The contraction in the muscles may be started by any form of ex- 
ternal irritation. A slight tap or pressure will sometimes bring on the 
slow, worm-like movement in them. 

Sensations are normal. Only a slight aching pain is complained 
of sometimes. The mind as a rule is more or less weak, though in 
some instances it is bright and clear. Epilepsy, hemicrania, pseudo- 
hypertrophy, polyneuritis, tetany and other neural complications have 
been observed with the disease. 

Diagnosis. — The diagnosis is not difficult as the clinical mani- 
festation is so unique. Diseases in which similar spasms occur are to 
be differentiated by the existence of other symptoms which myotonia is 
singularly free from. 

Prognosis. — The prognosis in regard to life is excellent. The 
disease is one of years and even a whole lifetime. It is not pro- 
gressive in the true sense of the word. Remissions may occur during 
Its course. 

Treatment. — There is no treatment that will prove of any avail. 
Gymnastics and constant activity helps to make life bearable bv keep- 
ing down the severity of the spasms. 



THE CHOREAS. 

The term chorea is from a Greek word meaning a dance, and is 
employed to indicate certain irregular, involuntary, incoordinated mus- 
cular movements observed in various disease states. It is therefore not 
a distinct pathological entity ; it is merely a symptom. This fact should 

be carefully kept in mind, as the underlying affection of which the 
choreic jerkings form one symptom is the indicator for the proper 
treatment to be employed, and not the choreic movements themselves. 



THE NEURONIC DISEASES 287 

The separating of idiopathic from symptomatic chorea, as some authors 
attempt to do, is entirely arbitrary and leads only to confusion. All 
the choreas are symptomatic, as will be seen in the further discussion 
of them. Acute minor chorea, the type of them all, is as much a mere 
symptomatic manifestation of an underlying toxaemia or other disease 
as are the choreas of hysteria, pre- and post-hemiplegic chorea, the 
pandemic choreas, Huntingdon's disease and the choreic phenomena 
associated with Friedreich's disease and other sclerotic processes. 

ACUTE MINOR CHOREA. 

Acute minor chorea, St. Vitus' dance, or Sydenham's chorea, is a 
disease of the central nervous system, frequent in childhood, charac- 
terized clinically by irregular, involuntary, incoordmated muscular 
movements, and by certain less obtrusive sensory and mental phenom- 
ena; and pathologically by a few scattered, circulatory, inflammatory 
and degenerative findings. 

Etiology. — Heredity does not play a direct role in acute minor 
chorea ; the so-called hereditary chorea, Huntingdon's chorea, is an 
entirely different affection. In almost one-sixth of the cases of this 
disease, however, a pronounced neuropathic taint is shown to run 
through the family. The child's forebears have been subject to epi- 
lepsy, insanity, hysteria, neurasthenia, narcotic poisoning with alcohol 
or tobacco, and even chorea itself. Race exhibits some influence, Jew- 
ish, German and Portuguese children being especially prone to the 
trouble. According to Weir Mitchell, the Negro race is singulany 
free from it. 

Later childhood is the favorite period for the outbreak of St. 
Vitus' dance ; and during this period girls are more frequently affected 
than boys, in the proportion almost of three to one. Nine-tenths of the 
cases, according to Gowers, occur between the ages of five and twenty. 
As puberty approaches the ratio of girls to boys increases. After 
twenty-five years of age the disease becomes more rare, and in old age 
it is very rarely seen as senile chorea. It is thus a disease of all periods 
of life, but especially of childhood, with a slight preponderance in the 
female. 

Ancemic, neuropathic and irritable children are often the victims 
of chorea and becoming hysterical, they sometimes manifest the com- 
bination of chorea and hysteria, which must always be carefully differ- 
entiated from the pure hysterical symptom known as chorea hysterica. 

The relationship between chorea minor, acute articular rheumatism 
and endocarditis is so striking as to call for more than a passing notice. 
It is estimated that approximately one-quarter of the cases of chorea 
give a history of acute articular rheumatism. The rheumatic symp- 
toms usually precede the choreic, though at times they may be coinci- 
dent with them, or even follow them. The rheumatic history is not 
so frequently obtained in the cases of early childhood as it is in the 
later and early adult cases. Another remarkable coincidence is the 
frequent appearance of endocarditis with chorea. Gowers affirms that 
it is within the truth to say that in one-half of the cases in which or- 



288 THE NEURONIC DISEASES 

ganic disease of the heart exists this preceded the chorea. Occasionally 
the heart lesion develops during the course of the chorea. So promi- 
nent is this relationship between the rheumatic troubles and chorea 
that many authorities, chiefly among the English and French, regard 
it as distinctly causal. German and American authors do not accept 
so strongly the relationship as one of cause and effect. 

Many explanations have been offered for this association of rheu- 
matism, endocarditis and chorea. Some say that chorea is merely 
rheumatism of the central nervous system. In other words, chorea is 
rheumatism, or rather one of the occasional symptoms of the general- 
ized trouble known as rheumatism, of which endocarditis and the 
articular swellings are also symptoms and complications. The absence 
of any distinct climatic influence upon the development of chorea, while 
on the other hand its proneness to appear in the spring and fall seasons, 
when it is known that rheumatism is most frequent, adds weight to the 
suggestion that chorea is largely a rheumatic symptom. It has been 
argued that the chorea is the result of the same toxic state of the 
blood that in all probability provokes the endocardial and joint inflam- 
mations. The existence of a specific microorganism (Richter, Berke- 
ley, Dana, Meyer, Pianese) has been invoked, after some observations 
and experimentation, to account for the toxaemia which institutes the 
chorea, and not a few believe that the same, organism will be found 
to be the cause of the rheumatism. Such a view receives some further 
support from the fact that chorea has developed during and after well- 
recognized infectious diseases, such as scarlet fever, typhoid, measles, 
pertussis, acute pyaemia, gonorrhoea, syphilis, puerperal fever and even 
the distemper. 

All of this makes of rheumatic chorea merely an associated mani- 
festation of a specific form of intoxication. It has this in its favor, 
that it is more plausible and founded upon better established observa- 
tion than is the older view that minute emboli from the diseased valves 
of the heart are floated up to the brain, where they become lodged in 
the finer terminal arteries, and produce areas of cerebral softening, 
which in turn produce the motor symptoms of irritation. 

Before leaving the subject of the relationship of rheumatism to 
chorea, let me warn against confounding all pains associated with 
chorea with rheumatic pains. Chorea is not solely a motor affection. 
but not un frequently shows implication of the sensory apparatus as 
well. 

Tt is a well-attested fact that a severe mental shock frequently 
results in an attack of chorea; and the effect of mental strain in school, 
worry, and otherwise, is undefinable. Osier says that the prominent 
psychical element in the causation of chorea is certainly one of the most 
serious objections to the infectious theory of the disease, since there 
can be no doubt that ordinary chorea may rapidly follow a fright or a 
sudden emotion. It is no objection, however, it seems to me, but rather 
a confirmation of the toxaemic theory. 

It is beginning to be well recognized now by alienists that changes 
in the blood, cither of a toxic character or at least affecting its metabolic 
function, may precede or follow sudden disturbances of mentalization. 



THE NEURONIC DISEASES 289 

The chorea from simulation, which has been observed endemically 
and reported from boarding-schools, etc., is like the true St. Vitus' 
dance epidemics of the Middle Ages. It is hysteria with choreiform 
manifestations. 

The occurrence of chorea during pregnancy is so grave a circum- 
stance as to demand a moment's consideration. Some think it is c. 
reflex chorea and is to be regarded in the same light as chorea rrom 
other peripheral sources, such as eye-strain, accumulation of wax in 
the ears, phimosis, intestinal parasites, etc. It is hard to imagine how 
a peripheral mechanical irritation can produce, by way of a reflex 
action, so unique and characteristic a symptom-complex as chorea is. 
Reflex action as a cause of disease has been heretofore too often ap- 
pealed to, and in view of many experiments and observations lately 
undertaken had better be dismissed except as a mere slight predispos- 
ing cause. In regard to the chorea of pregnancy, it is much more likely 
that an autotoxcemia is in some way responsible. This is shown by the 
fact that the chorea may appear before, during or after the pregnancy. 
The severity of the trouble and the frequent development of maniacal 
symptoms are also rather confirmatory. 

To sum up, the etiology of chorea, though varied and far from 
being established, points most suggestively to an infectious trouble 
associated with an unwonted mental strain, the underlying toxins af- 
fecting most vehemently the upper motor neurones and to a certain 
extent the sensory and psychic faculties, in that period of life, child- 
hood, and under that peculiar condition, neuropathic, when they are 
most susceptible. 

Pathology and Pathogenesis. — If we are contented with the 
view that chorea is merely a symptom of a more or less profound 
intoxication, the discrepancies in regard to the pathological findings 
may be easily accounted for. In a large class of cases there are no 
such findings and the disease is denominated functional. Unwonted 
susceptibility on the part of particular neurones in certain children, 
or the character of the causative infection, may well produce changes 
that will disturb the functions of those neurones and yet elude the 
power of our modern histological methods of examination. On the 
other hand, this infectious state, if sufficiently prolonged, or even the 
reaction caused by the violence of the disease in general, may lead to 
such scattered lesions as are sometimes observed at the autopsy. 
Of the latter there have been observed intense hyperemia of the brain, 
hemorrhagic and inflammatory foci, spots of softening, thromboses, 
emboli, etc., in the meninges, central ganglia and in the area sup- 
plied by the Sylvian arteries. Along with these circulatory findings 
must be mentioned the endocarditis, valvular disease and fatty degen- 
eration of the heart. 

All of these observations are inadequate as a basis for establishing 
a pathology of chorea, and thus regarding it as a distinct, uniform 
disease. The so-called chorea corpuscles are devoid of pathological 
interest in this disease, having been found in persons dead from other 
-causes (Wallenberg). 

Symptoms. — The most obtrusive symptom, and that which gives 



290 



THE NEURONIC DISEASES 



the name to this affection, is the irregular, involuntary, incoordinated 
jerking of the muscles. As it is the upper and not the lower neurones 
that are involved primarily, the jerking movements are not limited to 
individual muscles, but rather to groups of muscles, antagonistic or 
otherwise, that subserve generalized movements. Hence the head, or 
the arms, or the legs, or special parts of the body, like the tongue, the 
lips or the eyelids, twitch spasmodically. In other words, this 
symptom involves not muscles, but rather movements. For instance, 
the head will every few seconds jerk to the left or to the right; some- 
times it will be drawn backward or forward. The face will twist first 
to one side, then to the other; the lips will pucker or be drawn to 
one side; the eyelids will rapidly shut and open. All or any of the 
movements of the hand and arm may be affected. The thumb and 
fingers will snap shut and then open, or the whole hand will undergo 
a series of supination and pronation acts. The forearm may suddenly 
become flexed upon the arm and then relaxed, or the whole arm may 
be manipulated spasmodically from the shoulder. As with all intra- 
cranial or cerebral troubles, that part of the extremity in which the 
finer and more complicated movements take place normally will be 
more affected in the disease state. Hence the movements of the face 
are worse as a rule than those of the hand and forearm, those of the 
hand are worse than those of the entire arm, and the arms are worse 
than the legs. The trunk muscles usually escape, or when choreic 
movements attack them the disease is of another sort than the one I am 
describing. On account of the attitude of the patient, the jerking of 
the feet and legs is not so noticeable as that of the rest of the body. 
When the patient lies down or rests with the feet off the ground the 
leg movements become more obvious. With these movements ofttimes 
the whole body will be thrown violently about. 

This restlessness or incessant jerking may involve all parts of the 
body or only particular parts. It may therefore be confined only to the 
head or to one arm or one leg. More frequently it is bilateral in char- 
acter, implicating together the head, the two eyes, the two arms or 
the two legs. Occasionally the movements confine themselves to one 
side or the other, a condition known as hemichorea. 

The motor restlessness which comes on insidiously is peculiar in 
chorea and the symptom is not likely to be confounded with any other 
form of spasm. It is not rhythmical and it does not confine itself to 
any one muscle-group. It is now here, now there, rotating the arm 
or suddenly abducting and adducting it; then the legs jerk and cause 
the child to fall or at least to assume a disturbed gait. The entire body 
will turn from one side to the other. The eyes will twitch, the eyelid's 
snap, the tongue shoot in and out. The speech will be disjointed and 
difficult, and in extreme cases almost incomprehensible. 

These movements are all involuntary and are usually increased 
when under observation. The patient can control them 'for a few 
seconds, but not indefinitely. They occur mostly in daytime and dur- 
ing wakefulness. Sometimes they are present at night, during sleep. 
They are generally increased by associated voluntary movements,' 
though they themselves are always purposeless. Their constant vari- 



THE NEURONIC DISEASES - 29 1 

ability in form, direction and location is their most striking character- 
istic. 

Respiration is affected sometimes in so far as it is a voluntary 
process. The diaphragm is the respiratory muscle most involved. The 
muscles of simple phonation generally escape. 

The violence of these movements varies greatly in different cases. 
In some patients they are so slight as to be scarcely noticeable, and to 
be elicited in examination by the production of some emotional ex- 
citement only; while, on the other hand, they may be so general and 
terrific as to give rise to the distressing condition known as muscular 
insanity (folie musculaire ) , in which the patient hurls himself violently 
about, leaps up and down, injures himself, bites his tongue and 'finds 
it impossible to eat or get a moment's sleep. 

Muscular weakness is not uncommon. Sometimes it amounts to 
a mild paresis. The paralytic chorea of Todd is characterized by ex- 
treme paresis, with but few movements. Rarely after the attack a 
permanent, local paralysis or weakness remains. 

It has been stated by some that the disturbed action of the heart, 
sometimes observed, is choreic. This is scarcely probable. In some 
of the cases it is undoubtedly one of the signs of an endocarditis. The 
contractions that are said to occur in the papillary muscles are not 
based upon adequate demonstration. 

In most cases the above symptoms begin insidiously and are mild 
at first. Some are mild throughout the entire course of the trouble. 
Another class of cases become rapidly violent and continue so until 
the disease reaches its climax in about four or six weeks. Others are 
so frightful as to resemble acute mania of a most active type, and 
still others exhibit paralytic rather than choreic symptoms. It is ob- 
vious, therefore, that chorea as a symptom may vary all the way from 
mere restlessness or slight "fidgets," for which the child is too often 
punished, up to an extreme degree of muscular activity or paresis 
with mental aberration. There is no good reason, however, for classi- 
fying these various degrees of the trouble into the distinct types, mild, 
severe, paralytic, maniacal, etc., as some authors do ; for as the chorea 
is merely one manifestation of a complex symptom-group, dependent 
rpon various diffuse lesions of a more or less infectious origin, the 
classification might be carried on indefinitely, since no two cases are 
ever exactly alike. 

So prominent are the motor manifestations that many other symp- 
toms, almost equally important at times, are entirely overlooked, or at 
least not sought for. Among these sensation is included. Trousseau 
long ago used to declare that the sensibility of the skin is almost con- 
stantly disordered, and yet many authors to-day affirm that the sensa- 
tions are never affected. I have found present not only formication, 
tingling and other paresthesia, but actual pain of a neurotic origin. 
These slight, fugitive, muscular pains, sometimes sharp, but more fre- 
quently dull and aching in character, are, I am convinced, not unfre- 
quently mistaken for rheumatic pains. Headache is quite a frequent 
form of pain. It must be admitted that hyperesthesia and ancesthesia, 
hyperalgesia and analgesia, and all the intermediate sensory phenomena 



292 



THE NEURONIC DISEASES 



may occur with the chorea. In all probability the sensory symptoms 
are provoked in the same way, and probably by the same sort of lesions, 
as are the motor symptoms. 

Another set of symptoms too often passed by in the examination 
of a case of chorea are the menial. There is rarely a case in which 
some change of mentality does not occur. In the mild cases and in 
the beginning of nearly all the cases there is a peevishness, slight irri- 
tability, heightened emotionalism, weakness of memory, lack of con- 
centration and power of attention. These symptoms often show them- 
selves before the muscular jactitations attract attention, and bring down 
upon the child the anger and corrective punishments of school-teacher 
and parents. The other extreme of the mental picture seen in some 
rare cases includes violent delirium, shouting, singing, incoherent chat- 
ter and all of the usual exhibitions of a severe acute mania. Accord- 
ing to Fagge, Dr. Hills of the Norfolk County Asylum stated that more 
than one patient suffering from chorea had been sent to the institution 
as insane. Such errors are likely to continue to occur so long as chorea 
is regarded as a distinct, substantive disease, and not as a mere symp- 
tom which may be present in, and form part of, or at least be associated 
with, other forms of mental and nervous disease. 

The chorea may be the chief trouble and the psychosis a complica- 
tion, or, on the other hand, the primary trouble may be mental and 
the choreiform movements may be the passing complications. A 
careful differentiation, difficult to make at times it must be confessed, 
will be the only means of positively determining into which category 
the case should be placed. 

The most severe cases of the maniacal form of chorea occur in 
association with pregnancy. Sometimes they last for several weeks, 
the mania being noisy and violent for a time, and then subsiding into 
depression or apathy, with hallucinations, ideas of persecution, etc., or 
even acute paranoia. 

The special senses are usually not affected in chorea. In some 
children who, as a rule, are of the neurotic class, and therefore would 
probably have the same troubles with or without the chorea, there is 
hypermetropia, astigmatism and muscular insufficiencies. The fundi 
do not reveal anything particularly abnormal, although optic neuritis 
has been observed in a few cases. The pupils not unfrequently are 
dilated, but they react promptly both to light and accommodation. 
Irregularity of the pupils was once noted by Gowers, the larger one 
being on the side opposite to the limbs most affected. 

The deep reflexes are generally normal, but occasionally they are 
diminished, and cases have been recorded wherein they have been ab- 
sent. This symptom should not be given much stress, as the deep re- 
flexes are variable among people in perfect health. 

It has been argued by some that the joint changes, sometimes seen 
in choreic cases and formerly attributed to the rheumatism, are true 
arthropathies of the trophic sort. No other trophic symptoms of 
cerebro-spinal origin are observed in chorea. 

According to Osier, herpes zoster occasionally occurs, and other 



THE NEURONIC DISEASES 293 

skin eruptions, rheumatic in character, such as erythema nodosum and 
urticaria purpurica. 

As a rule the bodily temperature remains normal. A slight rise, 
however, is not especially exceptional. In maniacal chorea the tempera- 
ture may run as high as 104 degrees, just before death it has gone 
as high as 109 degrees. These elevated temperatures of chorea, even 
in the mild cases, are usually due to the complications, such as the 
joint affections, rheumatism or endocarditis. With the rise of tem- 
perature there will usually occur an increase in the pulse rate. The 
rapid pulse rate which some authors assign as a pure choreic symptom, 
indicating chorea of the heart muscle, is not necessarily associated with 
temperature. It is not due to chorea of the heart, but is merely the 
irritable pulse characteristic of neurotic children. 

In marked contradistinction to the renal function of hysteria, the 
urine of chorea is generally scanty in amount, high-colored and con- 
centrated and over-charged with phosphates and urea. Albuminuria 
is not a symptom of chorea, though it may be present when kidney dis- 
ease is complicating the trouble. In chorea nocturnal enuresis is not 
unfrequent. 

Chorea being a symptom merely) rather than a disease, it follows 
that it has numerous complications. Some of these are so frequent that 
they have been elevated by some authors to the dignity of special symp- 
toms. Such, for instance, are the heart complications. Others, I 
believe, are not so much complications of chorea as that the choreic 
manifestations are but additional symptoms of the diseases sometimes 
spoken of as the complications. This is illustrated well by some of the 
so-called rheumatic, syphilitic and other infectious accompaniments, the 
manias, and paralyses. This is a most important and practical distinc- 
tion to bear in mind, not only from the standpoint of diagnosis and 
prognosis, but especially from that of therapeutics. I will have more 
to say about it under the head of diagnosis. 

While at a loss to comprehend how the cardiac troubles, important 
as they may be, are to be considered among the symptoms of chorea, 
I will grant for the nonce that they may be complications and will 
discuss them under that head. It is my own belief that there is no 
direct relationship between the heart manifestations and the chorea. 
but that both are the direct result of the underlying toxic state of 
the blood, which toxic state of the blood sets up an inflammation in the 
one case and a functional neurosis in the other. 

Endocarditis is the most important heart complication. Pericarditis 
occurs occasionally. The former is almost invariably of the simple or 
warty form, according to Osier, and though not dangerous in itself. 
is apt to produce valvular incompetency. The usual sounds and signs 
of this heart complication are present. In chorea, however, there is an 
accidental heart murmur which must not be taken as indicative 
organic disease. It is anaemic in origin and is heard as a soft systolic 
blowing over the mitral and pulmonary valves. I have heard a l 
diagnostician assert that in his experience all cases of chorea exhibited 
heart signs, and upon the strength of this teach that chorea is always 
a rheumatic complication. Of the 140 patients with chorea examine* 1 



294 THE NEURONIC DISEASES 

two years later by Osier, the heart was found normal in 51, disturbed 
functionally in 17, and exhibiting signs of organic disease in 72. In 
my own study of 100 cases, about forty-nine per cent showed heart 
trouble, and not more than one-quarter revealed mitral insufficiency. 

The mistake of regarding chorea as always a disease with heart 
trouble as a complication is well shown in the attempt, first made by 
Kirkes and afterwards by able authorities, of explaining the neurosis 
on the ground of a local ischsemia caused by the presence of an embolus 
washed up into the cerebral circulation from the diseased valves of the 
heart. It is true, even as Oppenheim says, that in the course of chorea 
such an embolus takes lodgment and produces paralytic symptoms. A 
moment's consideration will convince any one that such a cause for the 
chorea most emphatically proves that the choreic jactitations are but 
a symptom of a much more extensive trouble. The chorea in such a 
case is of the pre- or post-hemiplegic type, and is but one of the symp- 
toms of one of the well-recognized forms of cerebral apoplexy. The 
disease is not chorea with embolic obstruction as a complication ; it is 
cerebral embolism with chorea as one of its accidental symptoms. 

Rheumatic manifestations in the joints, as well as generalized acute 
articular rheumatism, are sometimes put down as complications of 
chorea, and, strange to say, often by the very same authors who argue 
that chorea is the direct result of the rheumatism. It seems to me that 
this ready interchangeability of two such sets of phenomena as acute 
articular rheumatism and chorea minor is proof sufficient that both 
are but symptom-complexes, coincident and alike dependent upon infec- 
tion. This is further supported by the occasional, though rare, asso- 
ciation of simple neuritis. 

Among the psychoses and neuroses associated with chorea should 
be mentioned the maniacal manifestations, mild and severe, as already 
mentioned, hysteria and epilepsy. I recently saw a case of severe acute 
delirium of childhood, caused by some playmates throwing some earth- 
worms down his back, in which there were for several weeks gradually- 
fading frightful hallucinations with choreic jactitations. The chorea 
vanished before the hallucinations had entirely disappeared. Here 
again the mere symptomatic character o-f the choreic jactitations was 
made obvious and the impossibility of referring to the psychosis as a 
complication of the chorea or vice versa. Convulsive attacks, cataleptic 
in character, persistent spasms almost like typical hemiplegia, and even 
paralysis, are all seen sometimes in association with chorea. As many 
of these are of hysterical or organic origin, they should more probably 
be regarded as separate diseases in which the choreic phenomena play 
merely an accompanying role. 

Diagnosis. — In a simple, uncomplicated case the diagnosis of 
chorea is easy. The jactitations are characteristically irregular, involun- 
tary and incoordinate. As the term chorea, however, refers only to 
the muscular movements, the disease, if it is to be regarded as a dis- 
ease, is scarcely ever uncomplicated. It is these complications or asso- 
ciated symptoms that sometimes render the differential diagnosis diffi- 
cult. So far as the jactitations are concerned, it would seem hardly 
possible to confuse the choreic movements with the slow, wax-like 



THE NEURONIC DISEASES 295 

movements of athetosis, the rhythmical, somewhat more controllable 
movements of hysteria, the intentional movements of multiple sclerosis, 
or the peculiar tremor of paralysis agitans, etc. The distinction be- 
tween them will be pointed out under the head of these respective dis- 
eases. This distinction has only to be made, as a rule, in adults, as 
these latter diseases do not occur in childhood. 

There is a disease of childhood, the choreic athetotic form of 
cerebral infantile palsy, which may at times give much trouble. The 
muscular rigidity, particularly in the legs, associative movements and 
the athetoid nature of the twitchings will, if carefully sought for. 
be generally found and will indicate the cerebral palsy. 

Chorea has been mistaken for ataxia, especially when limited to 
the lower part of the body, and thus altering the gait. Oppenheim saw 
such a case in a boy three years old and was not led to make a diagnosis 
of chorea until he had observed the involuntary movements in rest. 

A general tic may be mistaken for chorea, or vice versa. The 
differentiation will be discussed under the head of the tics. 

Cases of Friedreich's ataxia were wont formerly to be reported as 
chorea. The slower character, athetoid-like jactitations of the former. 
the ataxia, the scoliosis, the scanning speech, the nystagmus and the 
familial nature of the disease, ought to make clear the differentiation. 

Choreic patients with marked maniacal symptoms have often 
been sent to the asylum as cases of insanity. The age in which insanity 
usually occurs, the garrulity and other mental symptoms and the rela- 
tive insufficiency of the muscular spasms will aid in making the diag- 
nosis of a primary psychosis. 

Prognosis. — The prognosis of chorea varies with the nature of 
the underlying cause. As a rule it is good, especially in those mild 
forms of the trouble known as acute minor chorea. These cases usually 
get well in two or three months. Occasionally they last only a few- 
weeks, and very rarely they last six months or a year, or even become 
incurable. The recovery, as a rule, is complete, but relapses are not 
uncommon. Only in the most violently severe cases, and even rarely 
in these, is the disease fatal. Death is the result of malnutrition caused 
by the inability to feed the patient. The dangerous signs of this seri- 
ous state of affairs are delirium, elevated temperature, irregular pulse 
and rapid emaciation. In most of these cases there is distinct heart 
trouble. 

About one-quarter of the choreas of pregnancy die, though the 
fatality is due to such factors as the severe psychosis, the cachexia, the 
heart complication and the abortion or unnatural parturition. 

Choreas late in life are more apt to become chronic or permanent 
than are those of childhood. Senile chorea is practically always per- 
manent. 

Treatment. — In the treatment of chorea three well-defined ob- 
jects are to be aimed at — the removal of the cause, the quieting of the 
mind and nervous system and the rapid nutrition of the patient. 

In most cases some form of infection will call for the first atten- 
tion. If it is rheumatism and its congeners, an antirheumatic line <>t' 
treatment is to be instituted, including; the regulation of the diet and 



296 THE NEURONIC DISEASES 

the use of such remedies as the salicylates, alkalies, iodides, cardiac 
remedies, etc. This is not the place to discuss the treatment of rheuma- 
tism, but it is pertinent to remark that the same treatment is to be 
employed in the management of rheumatic chorea. 

Other infections should be attacked in the same way. A syphilitic 
history calls for the iodides and mercury. Autointoxications should 
draw the attention to the emunctories. Cathartics, diuretics and dia- 
phoretics are all indicated in such cases. If a thorough and honest 
search is made for the cause of the chorea, predisposing or exciting,, 
organic, functional or reflex, and that cause removed, the disease will 
get well promptly and without further direct medication. 

In chorea, however, there is always a more or less exalted excita- 
bility of the mind and nervous system that needs particular care. The 
patient should be removed from all mental strain. He should be taken 
out of school. Threatenings and scoldings should be avoided. Even 
his games and playmates should be selected with the purpose of lessen- 
ing mental strain. In some instances seclusion for a time, with a 
well-selected nurse and the adoption of a modified Weir Mitchell 
treatment used for hysteria and neurasthenia, may prove most useful. 
Of this nature is a sojourn on a country farm or other change of 
residence. Of course, all stimulants, such as tea, corre-2 and alcohol,, 
are to be prohibited absolutely, and milk given in place of them. 

Hypnotics and sedatives, such as the bromides, come into play and 
ofttimes give the happiest results. In extreme cases chloral hydrate 
may have to be administered continuously and even continuous inhala- 
tions of chloroform. Morphine hypodermically and antipyrine have 
been borne well and given good results in a few cases of extreme sever- 
ity. The zinc salts, conium, cannabis indica, hyoscin, physostigmine,. 
exalgin, salol, salophen, etc., may all be tried, but will probably be 
found more or less unsatisfactory. 

The exhaustion, whether general or neural, whether a primary or 
secondary factor of the disease, is the condition that in many cases 
seems to demand the promptest attention. The best and the most 
rapidly acting tonics are here loudly called for. Of this class of reme- 
dies, arsenic still carries the palm. So prompt and generally satisfac- 
tory is the effect of arsenic upon the diseased neurones that it has 
come to be regarded as almost a specific in chorea. Any form of 
arsenic may be employed, though the favorite forms are arsenious acid 
and liquor potassii arsenitis (Fowler's solution). I prefer the latter. 
Beginning with a minimum dose, the remedy should be rapidly in- 
creased until the first signs of intolerance show themselves — namely,, 
nausea and oedema under the eyelids. The medicine should be dis- 
continued for a few days and then renewed, to be gradually increased 
again. In this way I have administered as much as twenty-five drops 
three times a day. Arsenical toxaemia can be largely avoided by ad- 
ministering it well diluted in water, and when there is food in the 
stomach. A few drops of mix vomica will cause it to be borne well in 
some cases. And as anaemia is so generally present, some form of 
easily assimilated iron may be judiciously given at the same time. I 
have never had herpes develop and I have never observed in my own 



THE NEURONIC DISEASES 297 

practice arsenical neuritis, though both are possible and have been 
reported. In some cases arsenious acid seems to act more powerfully. 
It is a convenient form to use with a chalybeate. 

OTHER CHOREIC DISORDERS. 

The desirability of dropping the term chorea as the name of a 
disease and of using it, like the term paralysis, merely to indicate a 
symptom, is shown by the multiplicity of choreas, spoken of in litera- 
ture and which, pathologically, ofttimes have absolutely nothing in 
common. We are not able to banish it entirely yet, because we do not 
know all that we should of these so-called choreas. Of the pre- and 
post-hemiplegic choreas, and one or two others, we have learned enough 
to cease speaking of them as diseases and to merely note the choreic 
manifestation as one of the symptoms of certain well-recognized patho- 
logical conditions. In time no doubt all the other choreas will be 
the same. Their division into essential and symptomatic choreas will 
do, temporarily, as a coarse classification, but it also will do when we 
learn positively whether the lesion is purely neuronic or extra-neuronic, 
whether the irregular, mcoordinated jactitations now referred to as 
choreic can be produced by intimate molecular changes in the nerve 
cells, as well as by the irritation of these cells by minute hemorrhagic 
inflammatory lesions. 

The former is what is meant to-day by essential, or idiopathic, 
chorea, and undoubtedly underlies the degenerative, hereditary, infec- 
tious and embolic types of the trouble ; the latter is referred to in the 
term symptomatic chorea. 

CHRONIC HEREDITARY CHOREA. HUNTINGTON'S 

CHOREA. 

Huntington, of Long Island, first described this affection in 1872. 
It was referred to, and probably Huntington's own cases described, by 
Waters in a letter to Dunglinson in 1842. In 1863 Lyon referred to it 
under the head of chronic hereditary chorea in a paper in the American 
Medical T lines. It is, therefore, not justly called Huntington's disease. 

It is an independent disease, with choreic manifestations prominent 
in its symptomatology and has no direct connection with Sydenham's 
minor chorea. 

It has been observed everywhere, here as well as in Europe, though 
it seems to be more common in and around New York. It is vulgarly 
called in the communities where it exists the "magrums" or "megrims," 
though it is as remote from migraine as anything possibly can be. 

The prime traits of the disease are its direct hereditary character. 
its late onset, its progressive, incurable nature and its association with 
pronounced mental deterioration. 

It is so distinctly recognized as a purely inherited disease tli.it 
children are interdicted in every possible way from intermarrying with 
families in which it occurs. Where a member <>t' an afflicted family 
escapes the disease and marries, his descendants, usually, though not 
always, escape also. 



298 THE NEURONIC DISEASES 

Literature contains numerous reports now of some remarkable in- 
stances of the disease and its hereditary origin. The reports of Zacher, 
Hoffmann, Lannois, Sinkler and some others are of special note. 
D'Ormea has described it in eleven members of one family of four 
generations. I recently saw a case whose father had had the disease, 
but could get nothing further of the history. The age of the patient, 
the choreic symptomatology and the marked mental deterioration were 
all typical. 

The disease appears so uniformly between the ages of thirty *a<3 
fifty that a member of a family cannot be said yet to have escaped it 
who has not arrived at that period of life. This late onset of the trou- 
ble is a marked characteristic and differentiates this from most of the 
other choreas of a general nature. It has been seen by Hoffmann, 
however, as early as ten years of age. 

It occurs about equally in both sexes. The families in which it 
occurs are strikingly numerous, eight and ten children being not un- 
common. In some cases it has started after a severe emotion. Gen- 
erally, however, there is no known exciting cause for it. When it has 
skipped a generation, epilepsy or hysteria has been seen in that gen- 
eration replacing it. 

The motor manifestations are typically choreic, consisting of ir- 
regular, sudden, incoordinate jactitations of all the muscles of the body. 
The arms and legs jerk and the face grimaces just the same as in 
ordinary minor chorea. 

The patient is to a certain extent rendered helpless by the move- 
ments when they are severe. His gait is affected, his speech is imperfect 
or even impossible, his respirations are embarrassed and he cannot use 
his hands in writing, hold knife and fork, etc. 

In mild cases the will can for a time repress the movements, but 
they are apt to be more violent elsewhere or later on. The reflexes 
are usually increased. 

The senses are not affected. 

The mind is always affected and its condition is one of the special 
features of the disease. There is a steady and progressive dementia, 
ending in complete idiocy in many cases. In the early stages, as in 
most dementias of the progressive, degenerative type, there is depres- 
sion, melancholia, suicidal tendencies and absolute apathy. The mental 
phenomena usually follow, though they may precede, the motor. 

The anatomical basis of the disease is unknown. In a few post- 
mortem examinations there were indications of a chronic meningo- 
encephalitis. Pachymeningitis, leptomeningitis, hemorrhagic foci, 
hydrocephalus and disseminated miliary inflammatory spots in the brain 
tissue were seen. The findings, according to Binswanger, were the 
same as in dementia paralytica. 

Some authors base their opinion upon these indefinite findings that 
hereditary chorea is pathologically a chronic meningo-encephalitis. 

It is hard to reconcile primary inflammatory changes with such 
pronounced direct heredity. To inherit inflammation and hemorrhagic 
foci without other cause for them is a new idea in pathology. 

In my own opinion the disease is a primary neuronic degeneration. 



THE NEURONIC DISEASES 299 

an inherited developmental defect. The gross findings referred to 
above are purely accidental and secondary. This, it seems to me, har- 
monizes both the indefinite character of these findings and the marked 
heredity in the disease. 

The patient never gets well, but steadily progresses toward idiocv 
and death. It may last many years, however. 

All treatment hitherto tried has proved futile, a result one would 
almost expect from the developmental character of the trouble. Were 
it a primary inflammatory trouble, some hope from treatment might be 
entertained, if not towards producing a cure, at least in checking the 
onward progress. Such a hope has never been realized. 

ELECTRIC CHOREA. 

Henoch, Dubini and others have described forms of choreic mani- 
festations that occur at various ages, sometimes endemically, in various 
parts of the body and are especially characterized by the quick, light- 
ning-like character of the movements. In Dubini's disease there are 
short, rapid spasms, that involve successively different parts of the 
body, painful sensations, epileptiform and even paralytic symptoms. 
There are often atrophy and electrical reactions present. Heart failure 
and coma usually terminate them. 

Recovery is exceedingly rare. 

Bergeron's electric chorea is hysteria. Henoch's electric chorea 
is in all probability a form of paramyoclonus multiplex observed in 
children. It is obvious that the sooner we get rid of the term electric 
chorea the better, for none of the diseases described under it are chorea 
or have any relationship to the genuine, irregular, incoordinated, non- 
sensitive jactitations of the latter. 

What is called habit chorea is a coordinated movement more nearly 
related to the tics. 

Chorea major is hysteria ; so is what is technically called hysterical 
chorea. Laycock's procursive chorea, wherein young girls exhibit 
rhythmical rotating and procursive movements of the body, is clearly 
hysteria. It has been called chorea festinans by some writers. 

PARALYSIS AG1TANS. SHAKING PALSY. PARKINSON'S 

DISEASE. 

This is a disease of advanced age characterized by a peculiar tine 
rhythmical tremor, muscular rigidity, with a more or less distinctive 
attitude, and a striking modification of the gait; without a known 
constant pathological basis; and without any encouraging amenability 
to treatment. The largest individual statistical studies of this disej 
have been made by Cowers upon i 15 cases seen in private and hospital 
practice, and by Hart upon 2\<) cases seen in the clinic of M. Allen 
Starr. Upon these reports, as well as upon a few personal observations. 
the following description is based. 

Etiology. — It is true that paralysis agitans is a disease of the 
aged, for rarely is a case seen under forty and most of them occur 



300 THE NEURONIC DISEASES 

much later. The decade between fifty and sixty is the favorite period 
for its appearance, about forty per cent, of the cases beginning then. 
Between sixty and seventy there were only twenty per cent, between 
forty and fifty, twenty-five per cent. Gowers says it is rare over 
sixty-five. It has been seen to occur as late as seventy-eight and per- 
haps later. 

That it is not solely a disease of advanced years is shown by the 
fact that Lannois recorded it in a child of twelve and Berger in a 
patient of seventeen. The youngest case that has been reported is that 
of Huchard in a child of three years. 

It is obviously a disease of the beginning degenerative period of 
life. 

Heredity seems to exercise so slight a role that it may practically 
be neglected. In about fifteen per cent, of cases a direct heredity has- 
been traced. A neuropathic tendency may underlie the disease and take 
the place of the direct heredity which is seen in the small number of 
cases so characterized. 

The influence of sex is probably not direct, but indirect, through 
exposure, occupation, etc. Males are afflicted with the disease about 
twice as frequently as females. 

The exciting causes that have been mentioned are numerous.. 
They include psychic shock and depression caused by worry, fright, 
anxiety, overwork, trauma, exposure, infectious diseases, such as 
grippe, malaria, typhoid fever, pneumonia, rheumatism, syphilis, poisons 
like lead and carbolic acid, intoxications with alcohol, tea and coffee, 
menopause, confinement, sunstroke, insomnia, abscess, piano playing, 
etc. As forty per cent, of the cases gave persistent worry as the prob- 
able cause, and as worry, dread and anxiety must have been more or 
less an accompaniment of the various other alleged causes, it may be 
assumed that psychic strain is the preeminent factor among the excit- 
ing causes. Many of the others may have paved the way for the gen- 
eral degeneration which seems to lurk beneath the disease process. 
On the other hand, it is always well to be mindful of the fact that 
worry is often a sign and result of, rather than a mere cause of, these 
degenerative troubles. 

The cause of paralysis agitans, therefore, it must be admitted, is 
obscure, though along certain lines a certain definite etiological picture 
can be outlined. 

Pathology and Pathogenesis. — Little need be said upon this 
subject, since so little is known, and what is known does not help very 
much in explaining the raison d'etre of the symptomatology. So far 
as any constant reliable findings, post-mortem, within the nervous 
structures are concerned, our knowledge is absolutely negative. The 
hypertrophy of the nerve cells of the pons Varolii described by Luys ; 
the induration of the pons, medulla and cord mentioned by Parkinson ; 
and even the more recent observations of Ketcher, Borgherini. Koller, 
Dana, Redlich and others involving sclerotic conditions of the blood 
vessels and the glia, and other findings similar to those noted in senile 
processes generally, are only worthy of historical interest. 

This total absence of any distinct discoverable lesions is remark- 



THE NEURONIC DISEASES 3OI 

able, especially in view of the fact that the symptoms are sometimes 
unilateral, monoplegic and otherwise indicative of a definite focal lesion. 
Gauthier seems to have hopelessly abandoned the nervous system en- 
tirely, for he looks upon the trouble as primarily one of the muscular 
system. Gauthier's position is not a plausible one, as Gowers has well 
shown. 

The character of the symptoms being so purely motor, and in a 
remote way similar to chorea, the source of the trouble must in all 
probability be looked for in the cerebral cortex and the motor centers. 
As Gowers well says, this is strengthened by the great similarity of 
these patients to a person under the excessive emotion of fear. There 
is a loss of inhibitory control with a regular explosion of abnormal 
nerve force from the lower cells, all due probably to certain physio- 
chemical intracellular changes as the result of a sort of senile-like 
degeneration and lowered nutrition. 

With Oppenheim, however, I agree that paralysis agitans should 
not be looked upon as a mere condition of presenility. It is a distinct 
disease of a more or less definitely localized pathogenetic process, and 
not a mere side issue to a general lowering of all the bodily forces and 
functions. 

Symptoms. — There are four special symptoms that characcerize 
•every case of paralysis agitans — namely, the tremor; the steady muscu- 
lar rigidity upon which the characteristic attitude depends ; the slightly 
paretic or retarded movements; and the gait. 

A typical case of the disease cannot be mistaken for anything else, 
-even at the first glance, for the symptoms in their combination are 
unique. With the head slightly bent forward and every joint in the 
arms, legs and body slightly flexed, the hands and arms trembling 
with a fine, rhythmical oscillation, the patient trips forward with a 
sort of mincing step, as if he were on the point of breaking into a run. 
The tremor and rigidity are usually seen in the same set of muscles. 
They may involve the entire body or only parts of the body. The move- 
ments of a voluntary sort in the arms and legs arc distinctly sluggish 
and delayed. 

I will now discuss the symptoms a little more in detail. 

The tremor is the special, obtrusive sign of the disease. It usually 
precedes, though it may follow, the appearance of the muscular rigidity. 
It may be limited to the fingers, which, being flexed, look as if the) 
were rolling a pea between them. It extends to the muscles of the 
arm or it may involve the arm and leg, usually on the same side. Winn 
all four extremities are involved, one side seems to be generally a 
little worse than the other. This characteristic one-sided distribution 
of the tremor, and its tendency to progress from the ends of the ex- 
tremities upward, indicates its hemiplegic nature and cerebral origin. 
The body sometimes oscillates, though for obvious reasons its tremoi 
is not so noticeable as that in the extremities. Some writers have de- 
clared that the head never shakes. That is certainly an error. I have 
seen it exhibit the same sort of tremor in both a to and fro and a rota 
tory manner, as the hands show. It is rare, however, in the head. Only 
in four instances among I I art and Starr's eases was the tremor) absent. 



302 



THE NEURONIC DISEASES 



That the parts of the body in which the voluntary movements are the 
most delicate and complicated are the preferential parts for the mani- 
festation of the tremor is shown by the greater number of cases that 
begin on the right side and in the fingers of the right hand. The 
upper extremities were involved seven times more frequently than the 
lower, and the right side a third oftener than the left. Sometimes the 
tremor advances very rapidly from one part of the extremity or body 
to another, at other times it will continue for years to be limited to 



FIGURE 41. 




Paralysis agitans. (After Charcot.) 

one part. Gerhardt and Hart both cite cases in which the tremor was 
intentional. 

In addition to the head, trunk and extremities, the tongue, the 
lips, the angle of the mouth, one side of the face, the eyeballs and the 
orbicularis palpebrarum have all been seen to be affected with the 
tremor. 

The tremor is a stereotyped one, fine, rapid and rhythmical. The 
oscillations are four or five to the second and the extent of the excur- 
sions is small. Sometimes the tremor is so fine that it is onlv observa- 



THE NEURONIC DISEASES 303 

ble in the patient's penmanship ; at other times it is very large and 
coarse. Voluntary active movements usually put a stop to the tremor 
for a few seconds. The same may be said of passive exercise and 
the fixing of the patient's attention. Mental excitement always in- 
creases the shaking. In sleep it usually ceases, but not in all cases. 
Neither the attitude of the patient nor the position of the limbs at all 
modifies it. At times it shows a tendency to remit. 

Next to the tremor the muscular rigidity is the important symptom 
of paralysis agitans. It usually coexists with the shaking and reveals 
itself about the same time. In some cases it comes on later than the 
tremor, in a still smaller number it even precedes the latter. Schlapp 
and Hart both report cases with rigidity, but without tremor. It is the 
muscles of the neck and back that reveal the rigidity, especially in the 
patient's stooping attitude. The slight flexion of the joints in the 
members affected with the disease is due to the muscular rigidity. 
When the face is involved the appearance is statuesque and wax-like 
indeed. 

The rigidity is noticeable also in the resistance offered by the 
muscles when passive motion is attempted. The same cause explains 
the delayed active movements. It seems as though the muscles could 
not respond as promptly as usual to the will. 

The modification of the gait is a. striking feature of the disease. 
The patient takes short, mincing steps on the tips of his feet and seems 
as if he were about to start into a run or to stride forward as though 
he were on the point of falling at every step. This is termed propulsion. 
Sometimes he exhibits a curious tendency to walk backward, retro pul- 
sion. Lateropulsion has been noted, but it is not common. Contrac- 
tures sometimes occur and incomplete paralysis in the later stages. 

The deep reflexes may be diminished or increased. They are often 
normal, never absent. There is neither atrophy nor electrical altera- 
tions in connection with the musculature. In two of Hart's cases, 
typical in every respect, the pupils were of the Argyll-Robertson type. 

The speech is often altered and there are changes in the voice. 
Slowness and irregularity, but not true dysarthria, scanning or stutter- 
ing characterizes the former ; while the latter *is monotonous and 
whining. 

Oppenheim says that hypcridrosis is rather a frequent occurrence. 
It does not bear any special relation to the parts affected with the 
tremor, though it may not be a generalized sweating. 

General restlessness is a characteristic in a goodly number of 
cases. This, however, may be due to the fact that active movement 
puts a certain amount of quiescence upon the tremor and so makes tin 
patient feel more comfortable. 

Among the sensory symptoms occasionally spoken of by these 
patients may be mentioned slight darting pains, aching, pricking, numb- 
ness, tingling and heat and cold, all very changeable, evanescent and 
subjective. 

The mind remains unaffected, or if it is affected it is a complication 
and not a part of this disease. Slightly depressive emotional states 
may occur, but as a rule the patients are cheerful and satisfied. 



304 



THE NEURONIC DISEASES 



FIGURE 42. 






Paralysis agitans. (From photograph in the Pathological Museum of the 
Med. Depart, of the University of Illinois.) 



THE NEURONIC DISEASES 305 

A slight elevation of temperature and an increase of the pulse rate 
have been observed in some cases. 

Diagnosis. — A typical case of paralysis agitans with its tremor, 
attitude, muscular rigidity, sluggish movements and peculiar gait can 
offer no difficulty in diagnosis. Other diseases may have a fon*i of 
tremor that may be suggestive of shaking palsy. Multiple scierosis has 
caused doubt in some instances. The earlier development of the dis- 
ease, the nystagmus, the intentional character of the tremor, the optic 
nerve involvement and the bladder disturbances wfll readily indicate 
the trouble as one of multiple sclerosis. 

Senile tremor is sometimes very much like paralysis agitans. The 
head is involved here more frequently and the shaking is always in- 
creased upon voluntary movement. Moreover, the other symptoms of 
paralysis agitans, the rigidity, the attitude, the gait are wanting. 

Oppenheim calls attention to senile paraplegia, a spastic paralysis 
of old age in which there is arteriosclerosis of the brain and cord, 
which presents a clinical picture not wholly unlike paralysis agitans. 
In the senile paraplegia, however, there are true paralytic symptoms, 
such as dysphagia, dysarthria, bladder disturbances, etc. 

Sometimes a form of traumatic neurosis occurs that is almost 
the counterpart of Parkinson's disease. These cases are difficult to 
differentiate at times, because it is a recognized fact that paralysis 
agitans sometimes follows trauma. However, in the traumatic neuro- 
sis hysterical or neurasthenic symptoms predominate and the charac- 
teristic symptoms of true paralysis agitans are not all present. 

Prognosis. — The prognosis of shaking palsy is good in regard to 
life, bad in regard to recovery. The disease usually involves the whole 
body in the course of a couple of years, then it may remain stationary 
for a great many years. Death often occurs from exhaustion. Apo- 
plexy sometimes closes the scene. A worse prognosis than death is 
that of the late paralysis, contracture and general bedridden, helpless 
state that sometimes obtains. Fortunately this is not a frequent condi- 
tion, in spite of the fact that the disease is most emphatically a pro- 
longed one. A mild delirium, a slight fever and a complete physical 
breakdown are the usual accompaniments of the end. 

Treatment. — The treatment of paralysis agitans is, if carried 
out on proper and conservative lines, attended with a fair degree of 
success, considering the chronicitv and fundamental nature of the 
disease. 

Mental and physical rest, quiet and nutrition are the main indica- 
tions of treatment. All sources of mental shock, disturbance and de- 
pression should be removed. Hence it is well to get these patients 
away into the country. Popular and fashionable resorts, sanatoria and 
all places where there is likely to be a crowd of people, with the at- 
tendant excitement, had better be avoided. Cheerful compan) . plea-ant 
occupation, light exercise, reading, simple games should all be urged. 
Good ventilation and a comfortable bed at night are important items. 
It is strange that because movement, such as carriage and railroad 
riding, makes these patients often feel better, as Charcot Ion- 



306 THE NEURONIC DISEASES 

pointed out, that any one should think of introducing vibratory chairs 
and other apparatus for their treatment ! 

The nutrition should be plain and abundant. Alcohol, tobacco, 
tea and coffee should all be discontinued. 

In the words of Oppenheim, all forced therapeutic measures should 
be avoided, such as cold water cures, massage, electricity, nerve- 
stretching, suspension. 

Purgatives, diaphoretics and antipyretics are of little benefit and 
may be dangerous. 

The following drugs have been recommended in this disease : 
Salicylates, Dover's powder, arsenic, Indian hemp, nitrate of silver, 
curare, bromides, atropine, phosphorus, cod-liver oil, picrotoxin. They 
are practically useless. The most advantageous medications are those 
that have a sedative and hypnotic influence. The hydrobromate of 
hyoscine, the sulphate of duboisine, morphine, codeine are the best 
of the palliative remedies. Podack recommends sparteine. Veratrum 
viride, gelsemium and nux vomica in the form of tinctures have quieted 
the tremor in some cases. Erb speaks highly of arsenic. My own 
experience inclines me to favor the hyoscine or duboisine. 

B. THE SYMPATHETIC NEUROSES. ANGIONEUROSES AND TROPHONEU- 
ROSES. 

ANATOMY AND PHYSIOLOGY OF THE SYMPATHETIC 

'nervous SYSTEM. 

The division of the nervous system into the cerebro-spinal and 
sympathetic is an artificial one. Both parts are intimately united 
anatomically and functionally and we cannot draw any sharp line of 
division between the diseases of the one or of the other. And it is 
probable that we never will, because it would seem, from both experi- 
mental and pathological observation, that the sympathetic merely regu- 
lates and controls in some way impulses that pass between the cerebro- 
spinal centers and the organs of vegetative life. In this fact, however, 
we can detect a slight specialization in the functions of the sympathetic. 
Symptoms of disturbance in the vegetative and nutritive organs indi- 
cate more or less involvement of the sympathetic, though doubtless 
conjointly with the cerebro-spinal apparatus. As the latter, however, 
cannot, it seems, produce certain manifestations without the conjoined 
activity of the former, we are justified in part in making a division be- 
tween cerebro-spinal and sympathetic diseases. The latter probabl> 
never occur without the former; the former very often occur without 
the latter. To illustrate, angioneurotic oedema is said to be a disease 
of the sympathetic nerve, but it always has associated with it cerebro- 
spinal symptoms. A localized myospasm is a cerebro-spinal nerve 
trouble, but it rarely has accompanying symptoms that point to the 
sympathetic. 

Much of our present knowledge of the Anatomy and Physiology 
of the Sympatlictic Nervous System we owe to the researches of Gas- 
kell, and in the following brief account I will follow his teachings. 



THE NEURONIC DISEASES 

FIGURE 43. 

Siwrior Cervical Ganglion of the Sympathetic; Its Connections and Branches. 

(Reduced from Flower.) 

ICtoIVC, Branches of commu- 
nication to lour upper cervical 
nerves. 

PS. Branches of communication 
to petrosal ganglion 

Vr, Branches of communication 
to ganglion of root of pneumogas- 
tric 

V, Branches of communication to 
gangnon of trunk of pneum >gastric. 

H, Branches of communication to 
hyp 'glossal nerve. 

C -\ Carotid plexus. 

C'P, Cavernous plexus. 

CA, Branches accompanying in- 
ternal carotid artery. 

OG, Branches to ophthalmic 
ganglion 

tk, To tympanic branch of glosso- 
pharyngeal. 

3, to third nerve 4, to fourth nerve. 
5, to fifth nerve, 6, to sixth nerve 

V, Vidian nerve to sphenopala- 
tine ganglion. 

S/», Large superficial petrosal 
from facial nerve. 

EAC, Accompanying branches 
of exiernal carotid artery. 

PP, Pharyngeal plexus, formed by 
union with branches of vagus and 
glossopharyngeal nerves. 

SG 7 Superior cardiac nerve. 
The Middle Ctrvical, or Thyroid 
Ganglion. 

IVC to VIC, Branches of com- 
munication with fourth, fifth, and 
sixth cervical nerve. 

IT, Inferior thyroid branches. 

MC, Middle cardiac nerve. 

ri , To recurrent laryngeal. 
The Inferior Cervical Ganglion. 

VI1C to VI1IC, Branches of 
communication with seventh and 
eight cervical nerves. 

IC, Inferioi cardiac nerve. 

C^, Cardiac plexus. 

GW, Ganglion of Wrisberg. 

LCP, Posterior, or left coronary 
plexus. 

RCP, Anterior, or right coronary 
plexus. 

CRL, Cardiac branches from 
pneumogastric or recurrent laryn- 
geal nerves. 

APP, To right anteiior pulmonary 
plexus. 

LPP, To left anterior pulmonary 
plexus. 

ID to IID, Branches of commu- 
nication from the first to the twelfth 
dorsal nerve. 

a, a, To a rta. vertebra, . oeso- 
phagus, and posterior pulmonary 
plexus. 

GSN, Great splanchnic nerve. 

SSN, Small splanchnic nerve. SSN', Smallest splanchnic nerve. D, Diaphragm. 

PN, Phrenic nerve. SP, Epigastii , or solar plexus. CLP, Cceliac plexus. C*, Cystic 

nerve. GSD. Gastro-duodenal plexus. CsP, Gastric, or coronary plexus. Pj>, Pyloric 
plexus. S/P, bplenic plexus. 1 GrE, Left g stro-epiploic plexus. Per, Pancreatic 

plexus. H/P, Hepatic plexus. V", Branches from pneumogastric. Dml\ Diaphragm- 
atic plexus. SG, Semilunar ganglion. SR*P, Suprarenal plexus. R»P, Renal plexus. 
S/P, Spermatic plexus. SMP, >ui eri^r mesenteric plex<i«. Met, Middle colic. Re/. Right 
colic. Ic/, ileo-colic. AP, Aortic plexus. IMP, Inferior mes>-nteiic plexus. LCI, 'e't 
colic plexus. Sz, Sigmoid plexus. SHw, Superior hem rrhoidal plexus IL to VL, 

Branches of communicati n with the five lumbar nerves. IS to VS, Branches of commu- 

nication with the five sacral nerves. C, Branches of communication with the coccygeal 

nerve. HP. Hypogastric plexus. IHP, Pelvic, or inferior hypogastric plexus, giving 
branches to all the pelvic viscera. 



307 




308 THE NEURONIC DISEASES 

The sympathetic apparatus consists of a double chain of inter- 
connected ganglia, lying on either side of the vertebral column and 
extending from the head to the pelvis ; of a number of more or less 
isolated ganglia, including the ophthalmic, the otic, the spheno-palatine 
and submaxillary in the head, various ganglia and plexuses in the 
thorax and abdomen, called cardiac, solar, hypogastric, aortic, sper- 
matic and renal ; and finally of various ganglia and plexuses in many 
of the viscera, such as the stomach, intestines and urinary bladder. 
Some physiologists regard the ganglia on the posterior spinal roots, the 
glossopharyngeal, vagus and sensory root of the fifth nerve as largely 
sympathetic in function. 

Rami communicantes, so-called, the visceral branches of the 
cerebro-spinal nerves, pass out from the latter into the lateral chain of 
the sympathetic, from which rami efferentes again emerge to enter the 
collateral ganglia, from whence pass still other branches to the various 
terminal ganglia in the organs of the body. Some fibres which can 
be traced back into both the anterior and posterior spinal roots are seen 
* to enter partly into the sympathetic chain and partly into the great 
splanchnic nerves. 

The white rami from the second to the fifth proceed upwards and 
join the superior cervical ganglion. Other white rami enter the lumbar 
and sacral plexuses. 

The gray rami do not represent, apparently, visceral branches 
below the second thoracic nerve-root and above the second lumbar. 

The white rami are, it would seem, the proper visceral branches. 
The white rami of the second and third sacral roots, however, com- 
mingle with the non-medullated fibres that pass from the ganglia to be 
distributed chiefly to the spinal column, the spinal membrane and the 
spinal nerve-roots themselves. 

All unstriated muscles receive branches from the sympathetic 
nerve ; hence all the viscera are innervated by it. The dilator of the 
pupil, the unstriated muscle of the lid, the erectores pilorum and the 
sweat and the salivary glands are all under its control. 

The cells are generally small and multipolar and possess an axis- 
cylinder process and numerous dendrites. The rami communicantes 
from the cord usually terminate in arborizations around the cell bodies 
in the sympathetic ganglia, making up thus the sympathetic neurones 
of the first order. The cell bodies lying in the sympathetic ganglia, 
with their neuraxones extending out to the unstriated muscles, con- 
stitute the sympathetic neurones of the second order. 

The following facts in regard to the distribution of the medullated 
visceral nerves emerging from the cord and entering the sym- 
pathetic and other nerves are of some clinical importance: They 
belong chiefly to the thoracic spinal nerve-roots. In the second and 
third sacral nerves they constitute the nervi erigentes, which pass 
directly to the hypogastric plexus and not into the lateral chain. From 
this plexus other fibres proceed to the inferior, mesenteric ganglia, to 
the bladder, the rectum and the generative organs. The white visceral 
rami of the upper cervical and cervico-cranial regions do not associate 
with the corresponding gray rami, but form the internal branch of the 



THE NEURONIC DISEASES 309 

spinal accessory nerve. This branch passes into the ganglion of the 
trunk of the vagus. Visceral fibres are found also in the roots of the 
vagus, of the glosso-pharyngeal and in the chorda tympani, small 
petrosal and other cranial nerves. 

The origin of these visceral rami is presumed for many reasons 
to be in the cells of the posterior vesicular column of Clarke in the cord. 
They are also probably connected with the cells of the lateral horn of 
the spinal gray matter and its representative in the medulla, the antero- 
lateral nucleus of Clarke. 

The efferent nerve fibres of the sympathetic supply the muscles 
of the vascular system with vasoconstrictor, vasodilator, cardiac ac- 
celerator and cardiac inhibitory branches ; the visceral muscles with 
viscero-motor and viscero-inhibitory branches ; and the secretory gland 
cells with their special branches. Their names indicate sufficiently 
their functions. 

Xot much is known of the functions of the sympathetic ganglia 
themselves beyond that of modifying the histological structure and 
maintaining the nutrition of the fibres that pass through and out of 
them. They are probably not reflex centers such as are those in the 
spinal cord. How much of the metabolism of the body is directly pre- 
sided over by the sympathetic nerve is not known. Gaskell believes 
that in it are anabolic and katabolic, constructive and destructive fibres 
respectively, which go to every tissue and gland in the organism. The 
functions of the system may be said in general to be motor, vasomotor 
and secretory. The last may also be trophic, though that is still an 
open question. 

Symptoms of Lesions in the Sympathetic Nervous Apparatus. — 
Some of these have been long known from early physiological experi- 
mentation. Bernard many years ago severed the cervical sympathetic 
and observed dilatation of the blood vessels on the same side of the 
head, with increase of cutaneous temperature, contraction of the pupil, 
and occasionally retraction of the eyeball. Stimulation of the nerve 
produced contraction of the bloodvessels, decrease of the temperature, 
dilatation of the pupils, dilatation of the palpebral fissure, protrusion 
of the eyeball and sweating, all on the same side of the head as the 
nerve stimulated. 

Lesions and diseases of the nerve in which disturbance of the 
physiological phenomena belonging to it have been noted arc numer- 
ous. Traumata, compression from neighboring neoplasms, apical in- 
flammatory alterations of the lungs and pleurae and abscesses are among 
them. The symptoms are both irritative and paralytic. In such dis- 
eases as glaucoma and exophthalmic goitre we. cannot, as W< 
points out, say there is any constant peculiar change in the cervical 
sympathetic. In the aged, the diabetic and the syphilitic, in leukaemia, 
pellagra, tuberculosis and infectious diseases, changes have been ob- 
served of the nature either of atrophy, hyperaemia, sclerosis, pigmentary 
and fatty infiltration, amyloid degeneration, accumulation of colorless 
blood cells and microccocci in the ganglionic blood vessels. We know 
scarcely anything of the diseases of tin thoracic or abdominal sympa- 
thetic, either pathologically or symptomatically. 



3IO THE NEURONIC DISEASES 

In associating the physiological disturbances sometimes observed 
in the vasomotor, cardiac and secretory spheres with disease of the 
sympathetic, one must remember that the same symptoms may be pro- 
duced by lesions in the cerebro-spinal system. Thus it is always an 
open question as to the exact location of the trouble in even fairly well 
defined sympathetic manifestations. Exophthalmic goitre, for instance, 
shows in many of its symptoms a possible relationship to sympathetic 
disease ; but those same symptoms might be well produced by a lesion 
in the cerebro-spinal apparatus, revealing themselves only secondarily 
through the sympathetic. 

The angioneurotic and trophoneurotic exhibitions generally are 
thus often only secondary sympathetic disturbances, the primary trou- 
ble being back in the cerebro-spinal apparatus. Tn universal inherited 
and acquired degenerative states, in general cachexia and infection, it 
would seem singular for the cerebro-spinal system to suffer and the 
sympathetic to escape. Hence we conclude that in these general neu- 
roses both parts of the nervous apparatus are implicated. We insist 
therefore that the nervous organism of the entire body is a unit and 
cannot be artificially divided physiologically as it is done anatomically. 
Among these sympathetic neurotic exhibitions we note flushing and 
pallor of the face, sensations of heat, rapid pulsations and excessive 
sweating. The heart palpitates, the head seems to suddenly fill up 
with blood, the ears ring, the eyes grow misty. It may be a sign of the 
sympathetic origin of these manifestations that through them all the 
conscious state is not disturbed nor are there any somatic muscular 
disorders or objective sensory phenomena. In hysteria, neurasthenia, 
profound nervous shocks, marked physiological strains such as puberty 
and the climacteric period involve, masturbation, sexual excesses and 
high mental excitement, the angioneurotic symptoms are not infre- 
quently observed. 

SYMMETRICAL GANGRENE. RAYNAUD'S DISEASE. 

This is a rare affection of the peripheral vascular system, charac- 
terized by a local asphyxia and gangrene, and dependent upon some 
disturbance of the vasomotor nervous apparatus. It occurs independ- 
ently or in the course of other nervous affections, such as hysteria, 
tabes dorsalis, syringomyelia, spinal tumor, epilepsy, exophthalmic 
goitre, scleroderma, etc. 

Etiology. — Heredity does not enter into its etiology, but a neu- 
ropathic constitution is probably a factor in every case. The young 
and middle-aged are most liable to it. Women are more frequently 
its victims than men. It has been observed in the nursing babe. A 
child three years of age completely recovered after losing, from this 
disease and spontaneous amputation, both arms above the elbow and 
the left leg below the knee. In children the disease occurs largely 
through the influence of the nervous system. In old people through 
the influence of the heart and circulation. 

Ancemia, chlorosis, exhaustion and physical defects, such as a 
congenitally small aorta, serve as predisposing causes. Exposure to 






THE NEURONIC DISEASES 311 

cold, emotional stress, suppression of menstruation and traumata of 
various sorts have been invoked as causes of the disease. It has 
followed various infectious and cachectic and debilitated states, such 
as malarial fever, rheumatism, neurasthenia. It has occurred in asso- 
ciation with tuberculosis and nephritis and in morphine and chloral 
intoxication. Diabetes and syphilis have been blamed for i- 

Pathology. — Of the pathology of Raynaud's disease we know 
very little. Raynaud himself suggested that there was a local spasm or 
contraction of the finer blood vessels. The smaller arteries are com- 
paratively abundantly furnished with muscular tissue and so are capable 
of active changes in their calibre. Their nerve-supply from the sympa- 
thetic is under the control of the spinal cord and is subject to influences 
in the way of cold, heat and dampness from the periphery, or from 
central disturbances caused by a toxic and vitiated state of the blood, 
or from an abnormal and unwonted impression sent down from the 
brain and the higher psychical centers. These provoke a spasm of the 
arteries and veins. An endarteritis and an endophlebitis have both 
been seen by Dehio, while Pitres and Vaillard have found neuntic 
changes in the nerves of the fingers. These were all probably secondary 
effects and have no bearing upon the pathogenesis of the disease. 

Symptoms. — The chief symptom of Raynaud's disease is a pecu- 
liar vascular spasm, appearing suddenly, paroxysmally and symmetri- 
cally at the ends of the limbs. Usually two or three fingers of both 
hands or several toes on both feet experience a paraesthetic sensation of 
some sort, crawling, numbness, deadness (digiti mortui). They as- 
sume a waxy paleness, are cold and look shrunken. Some anaesthesia 
is present and often severe pain precedes and continues during the 
onset. Blood does not flow if the fingers are pricked with a needle. 

This is the stage of local syncope or regional ischavuia. As a rule 
it lasts about an hour or so, and is then followed by a reaction in 
which burning sensation, redness and heat are observed. This may 
disappear in the course of a few hours more and the limb remain 
perfectly normal. More frequently, however, the syncope returns and 
becomes more of a permanent condition. 

In a few minutes or hours cyanosis or local asphyxia takes the 
place of the initial pallor. The skin becomes dusky, mottled, blue-black 
and finally black. The pains become intense and unbearable in tin 
hands and arms. Anaesthesia is not usually present, though it may be. 
The fingers are swollen and subject to slight hemorrhages and bullae. 
On account of the tension of the muscles and skin the lingers are stiff 
and awkward. The gait may he affected or the patient may not at- 
tempt to walk at all. 

Any part of the body may be the seat of these manifestations. 
Usually, however, they appear in the lingers and toes first, <>ih- finger or 
toe being affected sooner and more extensively than its neighbor. 
After the extremities the ears, the nose and areas of skin upon the 
arms and legs are involved. 

Such attacks may occur paroxysiually for years, being provoked 
by exposure to cold, as in winter, or by gastric . mental and other forms 
of disturbance. During all this lime the general health remains good. 



312 THE NEURONIC DISEASES 

More commonly this second stage of local asphyxia is followed by 
local gangrene. In the painful and mottled areas necrosis begins and 
may go on to the formation of complete sloughs, or it may retrograde 
and leave only a scar. Black spots first appear in the gangrenous areas, 
with vesicles and blisters which fill with bloody serum, burst and leave 
an exfoliating dark crust, or a slow-healing ulcer. The ulceration is 
superficial and when healed leaves a permanent scar. The repetition 
of this process leaves the tips of the fingers shrunken, irregular and 
unshapely from cicatricial formation. In severe cases, which, however, 
are rare, the necrotic process extends, mummifying the whole end of 
the finger or toe and establishing a line of demarkation at which 
spontaneous amputation may take place. Suppuration is slight and in 
the course of a little time the stump gradually heals. In this way a 
part of the foot or hand, the lobe of the ear, the tip of the nose or 
tongue may be lost. Symmetrica? areas upon the trunk ma}' be affect- 
ed and a condition even of multiple gangrene be set up. Such cases 
occur chiefly among young children, and on account of the intense 
suffering, the restriction of movement and the exhaustion, terminate 
in death in a few days. 

The relationship of hemoglobinuria to Raynaud's disease is re- 
markable and mysterious. It usually occurs in connection with the 
gangrenous stage. It may be present in the attack or it may take the 
place of an outbreak. The similarity of symmetrical gangrene and 
hsemoglobinuria is shown in the fact that both may be brought on by 
exposure to cold, the paroxysms often being preceded by a chill. In 
the one case the nerves and blood vessels are chiefly affected ; in the 
other the blood and blood-making organs. Albumin, haemoglobin, and 
red corpuscles are all found in the urine. Epilepsy has been seen in 
these haematuric cases. 

As a rule there is no fever, but the general strength and constitu- 
tional vigor are lowered by the continuous, unbearable pain, insomnia 
and loss of appetite. 

Mental dullness, temporary attacks of unconsciousness and other 
psychic and cerebral manifestations are not uncommonly observed. 
With depression they may even appear among the prodromes of the 
disease. Aphasia has been noted with transient right-sided hemiplegia. 
Delirium, delusions and mania must be added to the occasional cerebral 
manifestations. 

Sensibility is usually disturbed and conduction noticeably dimin- 
ished. Analgesia is probably the most common of the sensory modi- 
fications. Tactile sense is usually blunted, though the thermic sense 
remains intact. 

Trophic disturbances are exhibited in the ioint changes, including 
acute synovitis, swelling, thickening of the phalangeal articulations and 
anchylosis. These are multiple and attack several joints at the same 
time. Scleroderma may be associated with Raynaud's disease, and 
paronychia may develop between the attacks. The nails may be altered, 
the skin hypertrophied and the smaller muscles of the hand somewhat 
atrophied. 

Ocular disturbances, loss of hearing-, tinnitus aurium and modifier- 



THE NEURONIC DISEASES 313 

tions of taste and smell are not unknown, and sympathetic paralysis 
has been evidenced in certain oculo-pupillary phenomena. 

Thus the symptoms and complications of Raynaud's disease point 
to an implication of the entire nervous system. The immediate cause 
of the symmetrical gangrene, however, is obscure, though the indica- 
tions point to a functional instability of the vasomotor apparatus. 

The remote cause of this instability is in all probability a constitu- 
tional and neuropathic one; the immediate cause may reside in some 
form of disease in the peripheral nerves, the cord, the brain or the 
sympathetic system. 

Diagnosis. — The diagnosis of Raynaud's disease must take into 
account the early age of the patient, the bilateral and symmetrical 
character of the symptoms, the successive order of local syncope, 
asphyxia and gangrene, the implication of sensory, motor and trophic 

FIGURE 44. 




Raynaud's disease. (After Affleck.) 

functions and the absence of primary disease of the heart and blood 
vessels. It is not difficult in typical cases. 

Erythromelalgia is closely related to Raynaud's disease, but it 
never produces gangrene and the pains are usually relieved by cold 
instead of being made worse by it, as in the latter affection. 

Endarteritis obliterans does not present in successive paroxysms 
the syncope, asphyxia and gangrene observed in Raynaud's symptom- 
complex. 

In lepra mutilans several fingers are simultaneously and equally 
affected with gangrene and fall off without the presence of any pain. 

Neuritis is not paroxysmal nor gangrenous, though it may give 
rise to confusing trophic symptoms in the skin. Moreover, the etiology 
and symptoms of neuritis are so characteristically different from those 
of this disease that a differential diagnosis can usually be easily made. 

In senile gangrene the age of the patient, the presence of cardiac 
and vascular disease and the non-paroxysmal course of the trouble is 
to be remembered. 

Ergot poisoning resembles symmetrical gangrene in some resp< 
and Ehlers has argued that this and the allied tropho-neuroses wen- 



314 THE NEURONIC DISEASES 

all due to ergot intoxication. Tingling in the fingers and feet, cramps 
in the legs, arms and chest, dizziness and weakness, cold feeling all 
over the body, dilatation of the pupils and feebleness of the pulse, with 
retching, vomiting, diarrhoea and increased salivary secretion are the 
usual symptoms of ergot poisoning. Epidemics of gangrene have 
occurred from eating bread made from ergotized rye. 

Prognosis. — The prognosis is favorable in regard to life, except 
in the severe and multiple types of the disease. And yet patients even 
recover from these though mutilated and deformed. Death has very 
rarely occurred directly from this disease ; some complication has usu- 
ally been the cause of the fatal issue. 

No cure is known for it. Usually, therefore, it continues for years, 
appearing in periodical attacks. 

Treatment. — There is no known specific remedy. General hy- 
gienic measures must be instituted and the nervous system especially 
must be kept quiet and in a high state of health. The nutrition especial- 
ly must be maintained by gentle stimulation and abundance of easily- 
digested food. The bowels must not be allowed to become costive, the 
kidneys sluggish or the skin inactive. A regular and systematic out- 
door life and exercise must be adopted. The patient must be guarded 
from cold by suitable clothing and the removal to a warmer climate 
in winter. 

The administration of the iodides, chloral and nitroglycerin may 
be tentatively tried. Benefit from the nitrites is very doubtful. Hutch- 
inson advises the tincture of opium in three or four drop doses, three 
or four times a day, in combination with general tonics. Galvanism 
to the spine and sympathetic has been recommended. 

The pains are best combatted by local warmth, very gentle mas- 
sage and lukewarm hand and foot baths. Anodynes may be resorted 
to, but the hypodermic use of morphine may excite local gangrene. 
Cushing obtained relief from the intense burning pains, and improve- 
ment of the circulatory condition, by the gentle application of the 
tourniquet daily to one or the other limb, according as the symptoms 
indicated. 

ERYTHROMELALGIA. 

This interesting symptom-complex was described by Weir Mitchell 
in 1872 and named thus by him in 1878. Our knowledge of it is 
almost entirely clinical, in spite of the fact that there are now about 
fifty cases on record. It has been studied by Mitchell, Lannois, Collier, 
Hamilton, Sachs, Eisner, Rost, Dehio, Auerbach, Shaw and others. 
Mitchell regarded the trouble as morbus sui generis, but the opinion is 
growing that it is nothing more than a symptom of disease of the 
central nervous system, or peripheral arterial apparatus. 

Males are more frequently stricken with the trouble than females. 
The only known ec/uses for it are cold, a neuropathic diathesis and 
syphilis. 

The pathology of the trouble is but very little known and the 
pathogenesis not at nil. The only cases that have been examined 
satisfactorily post-mortem were those i^i Auerbach, Hamilton and 






THE NEURONIC DISEASES 315 

.Shaw. Edinger's findings in Auerbach's case consisted chiefly of r 
thickening of the intima and media of some of the distal blood vcsseis ; 
some degeneration in the nerve bundles of the cauda equina; degen- 
eration of the lower part of the posterior columns of the cord ; and 
some degeneration in the median part of Coil's column in the thoracic 
and cervical cord. The peripheral nerves were normal. In Sach's case 
the nervous tissues were normal, but the arteries were all diseased in the 
limb that was amputated on account of gangrene. In Hamilton's case 
there was some neuritic degeneration, but it was insignificant in coi. 
parison with the arterial disease. He concludes that the disease is more 
nearly related to Freidlander's obiiterative arteritis than to a degenera- 
tion of the spinal cord. Shaw's more recent findings lend support to 

FIGURE 45. 




Section of an artery of the great toe in Erythromelalgia. (After Mitchell 
-and Spiller.) 

this view. Nevertheless it is believed by many that erythromelalgia 
is a symptom-complex indicative of organic or functional disease of 
the central or peripheral nervous apparatus. By some it is considered 
to be an angioneurosis ; by others a disease of the posterior and lateral 
spinal gray matter. Plantar neuritis and acroneurosis are two other 
explanatory hypotheses. In view of its uncertain pathology and 
hypothetical pathogenesis, we must still look upon it as simply a re- 
markable symptom-complex. 

Burning pain and reddening of the skin in the feet, and more 
rarely in the hands, are its chief clinical manifestations. The pains 
usually appear suddenly, with or without fever, especially in the soles 
of the feet and in the hands and fingers. 'They may extend into tin- 
legs and arms. The parts soon become intensely red, hot and swollen. 
The blood vessels pulsate and there is local sweating. The pain is 
•of a burning character, usually .severe and even excruciating. It is 
more or less constant, though sometimes it remits. It is relieved by 
cold; aggravated by heat. Recumbency affords relief, whereas walk- 
ing markedly increases it. Standing increases the pain, the pulsation 
•of the arteries, the enlargement of the veins and the mottling of the 



3l6 THE NEURONIC DISEASES 

skin. (Edema is not uncommon. The objective sensibility is not very- 
much altered, though both hyperesthesia and slight hypaesthesia 
sometimes obtain. In this there is a suggestion of a peripheral neuritis.. 

Other symptoms besides these have been observed in conjunction 
with erythromelalgia, but they are not considered as part of the latter 
symptom-complex. There may be headache, vertigo, palpitation and 
attacks of syncope. Widespread arteriosclerosis and cardiac lesions 
have been found in some of the cases. Angina pectoris and functional 
disturbances of the heart have been reported in other cases. Unilateral 
sweating, thickening of the veins, enlargement of the bones, an atrophic: 
condition of the muscles of the limbs, hemiplegia, muscular dystrophy 
with cerebral tumor and other indications of disease of the centraL 
nervous system and of the peripheral nerves have all been noted in 
various cases. 

From the standpoint of symptomatology the conclusion of Lewin 
and Benda seems justifiable — namely, that there are among the re- 
corded cases three distinct classes: (i) Those with true organic dis- 
ease of the central nervous system; (2) Those with functional disease 
of the central nervous system ; (3) Those with peripheral disease of the 
nervous system, either functional or organic. 

Until more data of a pathological character are forthcoming to- 
uphold the view that this symptom-complex is dependent upon a 
primary disease of the arteries and their obstruction, we must accept 
the symptomatic evidence that it is a manifestation of some primary 
trouble in the nervous system. 

Obstinate and chronic, the trouble may last for years with remis- 
sions and exacerbations. The heat of summer aggravates it. During 
its course temporary convulsions and spells of unconsciousness have 
been witnessed. It is not dangerous to life in the absence of serious 
complications, but exhaustion, gangrene and complicating diseases add 
to the gravity of its prognosis. 

It is very resistant to all forms of treatment. Faradism, cold and 
the antipyretics of the coal-tar group have been tried for the pains. 
In exceptional instances warmth has seemed to give the most relief. 
In one case it disappeared after extirpation of the ulnar nerve. 

ACROPARESTHESIA.. 

This is a vasomotor neurosis of the extremities which sometimes 
may be regarded as a disease, though in the vast majority of cases it 
is a mere symptomatic trouble. Without objective signs of any sort, 
it leveals itself in paroxysmal attacks of numbness, tingling and other 
forms of paresthesia in the hands and feet. 

The condition was described by Putnam, of Boston, in 1880 and 
by Dana, of New York, in 1885. It remained, however, for Schultze* 
of Bonn, to name it acroparesthesia in 1893 and to awaken the pro- 
fessional interest in it. Many writers have since extensively treated of 
it, notably Laquer. Ormerod, Bernhardt, Berger, Friedman, Sinkler, 
Gallois, Charbo, Collins and others. 

Etiology. — Females are almost twice as often affected as males. 



THE NEURONIC DISEASES 317 

Most of them are about thirty or forty years of age. The climacteric 
seems to favor it. Nationality or occupation does not seem to have any 
special influence. The heredity, if any, is only that of a milol, general 
neuropathy. Convalescence from disease, a general cachexia and a 
state of debility have underlain it. Syphilis is not a cause. The things 
to which it has been attributed are so numerous that one is forced to 
the conclusion that none of them are causative except as mere excitants 
or as factors in producing a general nervous debility. In most cases 
no cause can even be suspected. Exposure to cold, sudden changes of 
temperature, as in laundry work with the hands, sewing, darning, long 
bathing, miscarriage, free use of alcohol and tea, fright, pregnancy and 
so on, ad infinitum, have been the antecedents of the trouble even as in 
all other neuroses. 

Pathology and Pathogenesis. — Of the pathology we know 
nothing, and of the pathogenesis we merely guess from the symp- 
tomatology that there must be a condition of irritation in the vasomotor 
centers which affects the nutrition of the peripheral sensory apparatus. 
Neuritis may be excluded, for it reveals none of the symptoms. All 
that we can say is that it is a vasomotor neurosis. Where the primary 
trouble is would hardly be worth guessing. 

Symptoms. — These are entirely subjective and sensory. They 
come on suddenly, often at night, even awakening the patient out of 
her sleep. The sensations are as varied in number as the patients 
themselves. The term paresthesia covers them all. Most prominent 
among them are numbness, tingling, formication, a feeling as if the 
limb, or rather more often, the finger-tips, were asleep. In rare cases 
the toes are affected. Sometimes the condition is actually painful ; at 
other times it is a distressing, itching, cold, wooden, swollen, stiff sen- 
sation. The movements of the extremity are usually restricted on 
account of the feeling. The trouble is more or less continuous, with 
exacerbations. It has been known to endure from a week to somewhat 
more than a year. The trouble may be confined to certain parts of the 
hand and foot, or to one hand. The rubbing and warming attitude 
and performances of the patient are characteristic. There are no uni- 
form objective signs; usually none at all. Sensation may be some- 
what decreased in the fingers or there may be a pallor. There are no 
motor disturbances. Other angioneurotic manifestations have been 
witnessed, such as the complaint of the patient of blood rushing 
to the head, of palpitation of the heart, etc. Tin- disease Is chronic, 
and, like all the primary neuroses, has an unsatisfactory prognosis. 

The diagnosis involves its differentiation from symptomatic 
paresthesia, from vascular disease and from other central organic and 
functional troubles. Care in the examination will make the differen- 
tiation easy, however. Raynaud's disease may simulate it. but there 
is local asphyxia and gangrene in this serious affection. Tetany, hys 
teria, acromegaly may all at times exhibit a resemblance t«. acroparaes 
thesia, but the appearance of other symptoms will soon distinguish 
them. 

Treatment. — Remove, of course, any discoverable cause. Gen 
-eral tonics, such as arsenic, phosphorus, strychnine, quinine and iron 



318 TllK NKUKONIC DISEASES 

are all useful on general principles in combating a neurosis. Ergotirr 
was recommended by Sinkler. Electricity in the form of central 
galvanization, medulla, cervical cord and sympathetic being brought 
within the current, and local faradization may be tried. 

ANGIONEUROTIC (EDEMA. 

Angioneurotic oedema, first definitely described by Quincke and 
his pupil Dinkelacker, is chiefly remarkable for the circumscribed 
swellings that appear on the face, neck and extremities, without ap- 
parent cause or previous warning. For this reason it has sometimes 
been called periodic swelling, urticaria tuberosa, giant swelling. There 
is almost always present gastro-intestinal disturbance, which is prob- 
ably of an (Edematous nature, like that of the exterior of the body. 
The mucous membrane of the larynx may be the seat of the sudden 
oedema and so cause an alarming dyspnoea or even death by suffocation. 

Etiology. — The etiology of the disease takes cognizance of the 
early adult age of the patient, its more common occurrence in the male 
sex, the occupations which tend to excessive fatigue of mind and 
body, and a certain natural or acquired neurotic state of the constitu- 
tion. Heredity seems to play an important role, as shown by the 
surprising series of cases, all in one family, reported by Osier and 
Milroy. In six generations of this family twenty-two individuals were 
the victims. Krieger's case was a young man twenty-five years of age,, 
whose mother was similarly affected. 

Cold and traumatism are frequent exciting causes of the attacks. 
The former in conjunction with lowered vitality may explain to a 
certain extent why, as in one of my own cases, the trouble was so prone 
to appear toward the early morning before the patient awakened. 
Unusual muscular exercise will sometimes precipitate an attack. I 
have seen a hard day's shopping, the patient passing from one store 
to another through the cold wintry air and climbing flights of stairs, 
do it. 

Alcoholism predisposes to this disease, likewise in some cases a 
sojourn near the sea. Nervous individuals are more frequently the 
victims. It has been observed in association with neurasthenia, exoph- 
thalmic goitre, hysteria and urticaria. 

Pathology and Pathogenesis. — The disease being so rarely 
fatal, very little opportunity has been afforded for making a thorough 
pathological examination. Its occurrence in markedly neurotic in- 
dividuals, and its many resemblances to a general neurosis, suggest 
that it probably has no discoverable lesion in the nervous system. It 
is probably related to hysteria, though the absence of the usual, well- 
known stigmata of the latter disease and other symptoms tend to prove 
that it is not pure hysteria. It is most likely a functional trouble of 
the sympathetic and central nervous apparatuses, but the cause and 
character of this trouble are, at the present time, entirely unknown. In 
this connection it is suggestive to note that Schlesinger reported a 
case in which this acute oedema was seen in combination with erv- 
thromelalgia and Raynaud's disease. Quincke himself regarded the 



THE NEURONIC DISEASES 319 

basis of the trouble as a vasomotor neurosis, the vessels being suddenly 
dilated. 

Symptoms. — The patient may be apparently perfectly well and 
remain indoors all day. Then upon going out into the open air toward 
evening, or upon taking a longer walk than usual, there may come 
on suddenly and without the slightest premonition an attack of 
dyspnoea, completely frightening and unnerving him. The extremities 
become cold, perspiration ceases, a slight cough arises and a feeling as 
if the stomach were suddenly distended. Then quickly follows the 
characteristic ccdematous enlargements upon the arms and face and 
elsewhere. These swellings are circumscribed and resemble giant 
hives, except that they neither itch nor give any pain. They measure 
from two to ten centimeters in diameter, are pale in color or of a 
deeper red than the surrounding skin. They do not pit upon pressure, 
like ordinary dropsical effusions, but if firmly pressed with the tip of 
the finger they quickly rise to their former level. Some patients com- 
plain of a local sense of burning or scalding, otherwise these tumefac- 
tions do not produce any distress. 

This circumscribed oedema, which may attack the mucous mem- 
branes as well as the skin and subcutaneous tissues, is to be differen- 
tiated in this disease by the abruptness of its onset, its brief duration 
and its rapid disappearance. Any part of the body may become its 
site, especially the face and extremities. In a migratory sort of a 
way it may vanish from one part, to quickly reappear in another, ft 
rarely lasts over a few hours. It is strictly non-inflammatory. 

It is probably true that the alarming dyspnoea and associated 
gastro -intestinal trouble are the result of the same oedematous process 
going on within the mucous membrane. Krieger's case, a typical one, 
was found dead in bed one morning and an autopsy showed that death 
was caused by sudden oedema of the glottis. Collins finds that out of 
seventy-two cases three showed their initial symptoms to be located in 
the stomach and in thirty-four per cent, of them all, gastro-intestinal 
manifestations were of sufficient importance to attract notice. The 
throat was involved in about twenty-one per cent, of all cases, a fact 
which should be carefully remarked, as death has more than once 
resulted from oedema of the larynx. The stomach symptoms arc, gen- 
erally, a sense of uneasiness and extreme tension, loss of appetite. 
enlargement of the epigastrium, colic and sometimes profuse vomiting 
and intolerable thirst. Osier says the pains may become so severe at 
times as to require the administration of morphia. 

In one of my cases there was at no time an) marked pain, but 
an intolerable sense of fullness and of retained undigested matter, with 
a bloated appearance of the epigastrium. 

Nausea and periodical vomiting may occur and are thought to In- 
due to the internal urticaria. The patients are usually constipated, 
though a colliquative diarrhoea sometimes follows the subsidence of an 
attack. 

Often the urine is voided in large amounts. Albuminuria 
casionally occurs and in one instance led to the* erroneous diagnosis of 
renal disease. Oppenheim saw a case where the suddenly appearing 



320 



THE NEURONIC DISEASES 



articular swelling simulated an attack of gout. Higier reported a 
case in which the oedema of the velum palati led to attacks that resem- 
bled pseudocroup. Hemorrhages have occurred from the mucous 
membranes and in one case Joseph saw a paroxysmal hemoglobinuria 
complicated with this disease. 

The frequent association of angioneurotic oedema with hysterical 
or hysteroid manifestations is striking. For a long time I regarded 
one of my cases as pure hysteria. In some cases, as in one reported by 
Collins, hysteric attacks preceded for some years the outbreaks of the 
cedematous trouble. 

Irregularities of the menstrual function seem to perform as much 
a part in the disease under consideration as they do in true hysteria. 
Collins, Lewin and Quincke cite instances in which the onset and dis- 
appearance of the migratory cedematous swellings bore a certain rela- 
tionship to menstruation. Amenorrhcea was sometimes accompanied 
by a monthly swelling of the ankles, lips or eyelids. 

Complete exhaustion and nervous anxiety often terminate an 
attack of the oedema. It was with great difficulty that one of my 
patients could be persuaded that her heart action was normal, so weak 
and prostrated did she feel when about to recover. Between the at- 
tacks the general health is good. 

Diagnosis. — The diagnosis of angioneurotic oedema is not dif- 
ficult if the characteristic symptoms are present. These symptoms 
are especially the local swelling of the skin, the gastro -intestinal dis- 
turbance and the nervous depression. 

Giant urticaria is a disease so closely related to angioneurotic 
oedema that some have thought they were the same. 

The ©edematous manifestations of hysteria are usually associated 
with the well-known motor, sensory and psychic symptoms of this 
latter disease. 

Prognosis and Course. — Angioneurotic oedema is rarely fatal, 
in spite of the severity of the attacks and the nervous depression often 
associated with them. The fatal cases that have been reported were 
probably due to asphyxia caused by the closure of the glottis from the 
cedematous swelling. This oedema of the glottis is to be dreaded as 
a possibility in all cases. One of my own, a woman, had been seized 
one night with one of her usual attacks and died of suffocation before 
the physician in the neighborhood summoned in the emergency was 
able to do anything. 

The disease is essentially a chronic one, lasting sometimes a whole 
lifetime. The general health is not greatly disturbed. 

While much can sometimes be done to lessen the frequency and 
severity of the attacks, the underlying constitutional trouble, the dis- 
ease itself, so far has proved intractable to all forms of treatment. 

Treatment. — No remedy has yet been suggested for its relief. 
Neither the disease itself nor the attacks arc amenable to any known 
treatment. The salicylates, especially the salicylate of soda, have given 
the best results in the hands of others, as well as in my own. By them 
the intervals between the attacks appeared to be lengthened, but as 
for lessening the severity of the attacks, or in any way actually pro- 



THE NEURONIC DISEASES 32 1 

<iucing anything like a permanent cure, I could not see that this or 
any other of the long list of remedies which I have experimented with 
were of the least avail. 

Special measures to regulate the digestion and bowels are, of 
course, always indicated. Baths, exercise, an even mode of life, the 
avoiding of all forms of mental and nervous strain go far towards 
ameliorating the trouble. 

Atropine and quinine have been lauded, though they were in- 
effective in my cases. Quinine is said to have produced a complete 
recovery in one instance, and in one of Oppenheim's it caused a rapid 
disappearance of the symptoms ; an assumption, however, hard to 
establish where the symptoms often disappear rapidly without any 
medication. Psychotherapy suggests itself in some cases on account 
of the close relationship of hysterical manifestations. 

CHRONIC HEREDITARY TROPHEDEMA. 

Meige recently described a remarkable series of cases, all in one 
family, to which he has given, for the disease, the above name. His 
first cases, reported in 1898, were two sisters, seventeen and twenty-one 
years of age. In both, at about the age of thirteen, a swelling began in 
the feet and gradually extended as far as the trunk. It was nor 
cedematous in the true sense of the word, for it was hard, did not 
vary with the elevation of the limb, and pitted only slightly after pro- 
longed heavy pressure. None of the ordinary causes of oedema were 
present. There were no signs of inflammation, no varicose veins, no 
pain. Xo other sensory symptoms, or motor either, for that matter. 
were present. A slight stiffness in the walk was caused by the tension 
of the parts. When Meige first saw the cases the mother of the girls 
was found to have the same condition well developed in both legs 
as far as the knees, and a brother beginning to reveal it in one lower 
extremity. The mother had had the trouble for twenty-seven years, 
without it causing her any special inconvenience. The grandmother. 
living at the age of sixty, showed the disease well developed in both 
legs, and the great-grandfather had suffered from it. Two maternal 
uncles of the two sisters first seen, dying at the ages respectively of 
twenty-five and twenty-seven, had been victims of the disease also. 
In Lartat-Jacob's cases of two children, aged respectively five and ten 
months, a similar condition was seen. Not only was the oedema con 
genital, but also hereditary, as shown by the fact that the maternal 
grandmother, her sister, her brother and a first cousin of die little 
patient's mother all had the disease. Similar cases have been reported 
by De Rove and Mover. 

[INTERMITTENT ARTICULAR HYDR< >PS. 

This is a condition referred to by Moore, who first described it. 
by Oppenheim, by Fere and others. Usually the knee, sometimes the 

other joints of the extremities, the spinal column or the maxillary 
articulations are effused with fluid regularly every few days or weeks. 



322 



THE NEURONIC DISEASES 



A mild fever has occurred in some cases. There are absolutely, how- 
ever, no other local or general symptoms. It is said to be an inde- 
pendent disorder or an accompaniment of one of the general neuroses, 
like exophthalmic goitre. Fere has described a permanent hydrops. 
The disease has been associated with trauma, malaria and other causes 
without good reason. It has no relationship to rheumatism, but is a 
pure neurosis. It is obstinate, but sometimes goes away of itself or 
alternates with polyuria, hyperidrosis or the symptoms of exophthalmic 
goitre. 

Treatment is not satisfactory, though it includes the salicylates, 
arsenic, quinine, ergotine, laxatives, electricity and hypnotism. 



EXOPHTHALMIC GOITRE. 

This is often called Graves' disease because this English practi- 
tioner wrote a clinical account of it in 1835, which attracted the atten- 
tion of the medical world. On the Continent the name of Basedow, 
of Germany, is usually employed, because he described it independently 
in 1840. If any physician's name is to be attached to it, that of Parry 
has the strongest claim, since he has left in his posthumous writings 
a very fair clinical portrayal of his first case, seen in 1786, and others 
observed later. The contention of the Italians that Flajani fully de- 
scribed it in 1800 is not well substantiated. 

Our present knowledge of the affection does not permit of its 
exact classification. Clinically it is a neurosis. Pathologically and 
pathogenetically there is some ground for suspecting that it is a 
thyroid disease. A strict definition, therefore, can only include a 
few meager facts in regard to its etiology and the symptom-complex 
tachycardia, enlarged thyroid, protrusion of the eyeballs and certain 
neurasthenic and vasomotor manifestations. 

Etiology. — Heredity enters as an important factor in the etiology 
of Graves' disease. In a few instances it is direct. A mother and two 
sons under my care have had it, the latter recovering completely. In 
another instance an aunt of the patient suffered from it. Similar 
examples have been observed and reported by others. In the majority 
of cases, however, the heredity is only indirect. Various other neu- 
roses, such as neurasthenia, chorea, epilepsy, hysteria, psychoses and 
nervous strains from excessive indulgence in alcohol and tobacco, can 
be recorded in the family history. A neuropathic condition is trans- 
mitted to the offspring and through the female line. The affection is 
sometimes called a "woman's disease," as it has been observed to 
occur ten times more frequently in women than in men. 

It appears at all periods of life, but most commonly in the second 
decade of women, and the third of men. Worry, fright, anxiety and 
extreme emotional depression have often been observed to precede it, 
but whether they were causative or symptomatic has not always been 
clear. All exhausting influences, general debility and anaemia predis- 
pose toward it. T have seen cases that followed pregnancy, abortion, 
the puerperinm and prolonged spells of illness. Abnormal menstrua- 
tion, cardiac disease, infection (scarlet fever, rheumatism, pneurrlonia, 






THE NEURONIC DISEASES 323 

syphilis, etc.), diarrhoea, excessive use of alcohol, over-exertion, like 
mountain-climbing, and injuries to the head, have at various times 
been assigned as causes. 

If exophthalmic goitre is primarily due to disease of the thyroid 
gland, some of the above-named factors cannot reasonably be looked 
upon as causes, much less as symptoms. And yet they are too fre- 
quently and too intimately associated with it to be regarded in the 
mere light of accidents or coincidences. As etiological factors they 
can fit in with the conception of the disease as a primary neurosis — a 
conception which is further supported by such elements in the etiology 
as the sex, age and heredity. 

Pathology axd Pathogenesis. — The post-mortem findings are 
so indefinite that even at the present day nothing but hypotheses can 
be offered in explanation of the nature of the disease. Among the 
various theories only two are worthy of special consideration — namely, 
the one that regards the trouble as a primary neurosis, and the other 
that looks upon it as an intoxication from primary disease in the thyroid 
gland. 

In the former theory it is assumed that there is a functional dis- 
turbance, toxic or quasi-physiological, within the cellular elements of 
the central nervous apparatus, and that ail of the symptoms of the 
disease, cardiac, glandular and ophthalmic, are the direct result of the 
neurosis and are in no way dependent upon one another. Attempts 
have been made to localize the neurotic process in the medulla ob- 
longata (Filehne, Durdufi, Bienfait, Sattler, Fitzgerald), the cerebral 
cortex (Newman) or the peripheral apparatus, including especially 
the vasomotor sympathetic system (Abadie). None of these efforts 
have proved successful. The immediate cause of the neurosis is wholly 
unexplained. 

The other theory of the disease is the so-called "hyperthyroida- 
tioir' or "dysthyroidation" theory. It was first promulgated by 
Mobius, of Berlin, in 1886, and has been ably supported by Wette, 
Muller, Jofrroy, Brissaud, Segnault, Boinet, Bramwell, Murray, Adam 
and Greenfield. As a result of disease in the thyroid gland, an exces- 
sive or altered secretion is poured out into the circulation and this, 
either by its direct toxic effect or by its disturbance of the general 
metabolism, causes all of the nervous manifestations and their 
ondary results. 

Chronic iodism or thyroidism, depending upon the thyroiodin or 
iodothyrin, a normal substance found in the gland, both free and in 
combination with a proteid and containing 9.3 per cent, of iodine and 
0.56 per cent, of phosphorus, is believed to be the essential trouble. 

The origin of this glandular disease is not explained, though a few 
authors fall back upon some form of nervous trouble, possibly a neu- 
rosis, in accounting for it. This thyroidation theory i^ popular just 
at present; is supported by various more or Jcal arguments; 

and affords a basis for the surgical treatment of the di& 

Hypertrophy and persistence of the thymus gland has often been 
seen. The other pathological findings, such as the degenerative changes 
in the sympathetic, the inflammatory and other foci of disease in the 



324 THE NEURONIC DISEASES 

restiform bodies and elsewhere, and even the cirrhosis, hyperplasia and 
vascular alterations in the thyroid gland itself, are scarcely constant 
and decisive enough to be regarded as the histopathological foundation 
for the disease. 

Until more constant post-mortem evidence to the contrary is 
forthcoming we must still regard exophthalmic goitre as a mere symp- 
tom-complex and largely of the nature of a neurosis. The numerous 
hypotheses put forth to explain its pathogenesis, while interesting and 
suggestive, are none of them established as positive facts. 

Symptoms. — The onset of the disease varies. After some un- 
wonted exertion, hemorrhage or mental shock the symptoms may 
promptly appear and rapidly increase. After some prolonged physical 
strain, worry or infectious disease they usually come on gradually and 
develop slowly. Once developed they are more or less permanent, 
though they may be subject to occasional remission. In some mild 
cases they quickly appear and disappear. In the acute severe cases 
they usually subside somewhat and the disease becomes stationary and 
chronic. 

The clinical presentation of Graves' disease includes the tripod of 
symptoms tachycardia, struma and exophthalmos. Not all of these 
are present in every case, nor are they all equally prominent when 
present. There are other symptoms that are almost of like importance, 
as, for example, trembling, hyperidrosis and mental depression. After 
these are a long list of neurasthenic and hystero-neurasthenic mani- 
festations in regard to which it is not always easy to say whether they 
are symptoms or complications. 

The tachycardia, or irregular rapid action of the heart, is the 
earliest, the most constant and subjectively the most obtrusive of all 
the symptoms. So pathognomonic is it that when it cannot be account- 
ed for on the basis of any other organic or functional heart disease, a 
diagnosis of incipient exophthalmic goitre is allowable. It may come 
on abruptly or gradually. Often it is the only symptom that sends the 
patient to his physician ; at other times it is only discovered as the 
result of a most painstaking examination. The phenomenon is like 
that which occurs when a person is unduly excited. Subjectively the 
heart seems to throb violently and spasmodically without rhyme or 
reason. Nervous excitement may induce an exacerbation or increase 
it. Objectively it is observed to beat irregularly and with an exalted 
degree of force. In bad cases it flutters and pounds and seems like 
a caged animal struggling to set itself free. The impulse is sharp and 
noticeable over a wider area than normally. In mild cases the beats 
number about 100 to the minute; in the majority of the cases it rises 
to 120 or 140; in the more severe cases it may even go to 200. Rarely 
docs it ever subside to the normal, except in the mild cases. Some- 
times the pulse is regular and small, while the arteries beat vigorously. 

With all this energy the circulation is not actually hastened. The 
condition is merely a sort of delirium cordis, representing not strength. 
but rather lack of inhibition. 

Usually there is no indication of an organic lesion upon physical 
examination. Slight enlargement of the heart may be detected later 






THE NEURONIC DISEASES 325 

on, this being clue to dilatation rather than to hypertrophy. Occasion- 
ally a systolic murmur is heard near the base of the heart. Graves 
stated that in one case this was audible at a distance of four feet from 
the patient. As the result of the dilatation a sound suggestive of 
mitral regurgitation may be heard at the apex. All of these are sec- 
ondary manifestations and when dependent upon actual organic lesions 
are to be looked upon as complications. Valvular defects from slight 
endocarditis have been occasionally found post-mortem. 

Severe paroxysms of palpitation, extreme violence of action, accom- 
panied by dyspnoea and signs of dilatation, without hypertrophy, are 
among the later cardiac manifestations. The arterial system becomes 
dilated from the lowered tone of the vascular walls and the increased 
pulsations of the heart. The carotid arteries especially, the thyroids 
and even the abdominal aorta, exhibit an exalted pulsation. A loud 
systolic murmur may be heard in the neck and is rarely ever entirely 
absent. A curious fact is that the smaller arteries beat comparatively 
less forcibly than the larger-sized vessels. The entire arterial system, 
however, is subject to the peculiar throb. In a few instances, which 
are exceedingly rare and in which the thyroid was markedly enlarged 
and variable, the exophthalmos slightly observable, and the tremor, 
sweating and neurasthenic symptoms were present, I could not detect 
the slightest alteration in the heart action. These cases sought medical 
advice solely on account of the increased size of the neck. 

Xext to the heart phenomena the enlargement of the thyroid gland 
is the most frequent and important symptom. Occasionally, as I have 
seen, the first and only thing to attract the patient's attention is the 
increasing tightness of her collar. In one or two instances the friends 
detected the enlargement before the patient did. Objectively it is the 
most noticeable symptom, and as it appears sooner or later in almost 
every case, it is to be regarded as a cardinal symptom. 

Those who believe that the thyroid is the primary scat of the 
entire disease find some difficulty in explaining the cases in which it 
fails to enlarge, and in the exceedingly uncommon cases in which it 
actually diminishes. They are driven to assume that the gland is 
just sufficiently diseased to produce an abnormal secretion without be- 
ing itself altered in size. 

The enlargement of the gland is gradual and slow. It begins 
usually after the tachycardia has existed for some time. It is not a 
uniform enlargement. Most frequently the right side is bigger than 
the left. Tt may be equal on both sides. The isthmus is rarely in- 
creased. Sometimes there are remissions, or rather the gland alter- 
nately enlarges and recedes. Later on it becomes permanent. The 
patient realizes the change in the gland by the tightness in her dl 
and occasionally by a distressing sensation as though something were 
about to choke her. The degree of enlargement is usually not ex- 
cessive and very rarely as much as it is in ordinary goitre. Tin- super- 
ficial veins over the gland are dilated. Palpation sometimes reveals 
a slight thrill and auscultation enables one to detect a soft, blowing 
murmur synchronous with the- cardiac systole. ( iuttmann decla 
that a double murmur is pathognomonic. 



326 



THE NEURONIC DISEASES 



The protrusion of the eyeball is a variable symptom, though highly 
characteristic of the disease when present. It is the least frequent of 
the three cardinal symptoms and it is often entirely absent. It usually 
appears with the enlargement of the thyroid. It rarely occurs alone. 
It may be unilateral, more commonly it is bilateral. The right eye 
is apt to be a little more prominent than the left. Generally the 
condition is slight and sometimes it is barely noticeable. It may be so 
marked, however, that the insertions of the recti muscles may be 

FIGURE 46 




Exophthalmic goitre. (Eisendrath.) 

exposed. The lids are drawn back, the white sclerotic coat is widely 
visible and the patient exhibits a highly exaggerated surprise-look or 
stare. The movements of the eyeball are limited, the lids cannot close 
and the conjunctiva is slightly irritated. The eyeball is actually in- 
creased in size somewhat and may be painful as well as prominent 
Vision is not generally disturbed, though myopia has occurred, prob- 
ably on account of the increase in the size of the globe. The fundus 
appears normal, though the retinal arteries may pulsate abnormally. 
Secondary effects, like ulceration, sloughing and opacity of the cornea. 



THE NEURONIC DISEASES 



327 



have followed the insufficient protection of the eye. (Edema of the 
lids and even optic atrophy have been observed. 

A remarkable symptom, which, however, is only present when 
there is exophthalmos, is that known as Von Graefe's. If the patient 
holds her head still and is asked to follow with her gaze the finger of 
the examiner, carried slowly downward about twelve or fourteen 

FIGURE 47. 




Exophthalmic goitre. (Colburn.) 



inches in front of her eyes, it will be noticed that as the ball of the 
eye rolls downward the upper lid fails to follow it as it docs in health. 
This is not due merely to the physical obstruction, for the symptom 
does not occur when tru are protruded from any other cause. 

The upper lid is in a state n\ spasmodic elevation from implication of 
the fibers of the muscle of Miillcr. The presence of this symptom is 



328 THE NEURONIC DISEASES 

therefore dependent in no way upon the exophthalmos and consequent- 
ly may be observed when the latter is very slight. It is usually bilat- 
eral and may vary in degree of severity. 

Winking does not take place as often as it does in normal indi- 
viduals (Stelhvag's symptom), and there is some retraction of the lids 
so that even in the mildest cases of exophthalmos the palpebral fissure 
is wider than would be expected. 

The internal rectus of one eye may be weakened, as shown by 
asking the patient to look at the tip of his nose. External ophthal- 
moplegia has been observed, though as a rule there is no paralysis of 
the ocular muscles in this disease. There may be a vibratory tremor 
of the eyeball, as is sometimes seen in other parts of the body. Lacry- 
mation may be a symptom. 

So constant is tremor that some authors add it to the three cardinal 
symptoms of the disease. I have not found it so frequently as this, 
though I have seen it many times. Basedow first described it. The ex- 
tremities and the head oscillate with a fine, regular movement, eight to 
ten oscillations to the second. As the symptom usually occurs early 
in trie disease, and does not always continue throughout its course, it 
is important always in the diagnosis. It is suggestive of the tremor 
of paralysis agitans. Mental excitement and exertion increase it, but it 
is never absent even during rest. Choreiform jactitations have been 
occasionally noticed in conjunction with this tremor. 

In addition to the four important symptoms of exophthalmic 
goitre just described there are many others, less constant, but often of 
much assistance in arriving at a diagnosis. Among these hyperidrosis 
has seemed to me to be ratlfer frequent. Nearly all of the patients 
complain of sweating more than they have been accustomed to doing, 
especially under the arms. Sometimes it is unilateral and even local, 
as in the palms of the hands, about the head, etc. On account of this 
dampness of the skin the local resistance to the electric current is 
markedly diminished. 

A psychosis of some sort is nearly always noticeable in exoph- 
thalmic goitre. It may amount only to a slight degree of irritability, 
anxiety, restlessness and melancholy — a mild phrenasthenia. The 
memory, the power of attention and the will may be somewhat weak- 
ened. Sleep may be disturbed so as to be either very light or very 
profound. Unpleasant dreams are not uncommon. In rare cases 
actual delirium, mania, melancholia, with distinct hallucinations and 
illusions, may break out. An effort must always be carefully made to 
determine whether the psychosis is primary or secondary. Exoph- 
thalmic goitre occasionally occurs among the insane. The psychosis 
that is a symptom of Graves' disease usually assumes an atypical form 
and its course is variable. Acute mania may appear and terminate in 
death in a few days. 

The general health of these patients is usually deteriorated. They 
are anaemic, weak, emotional and emaciated. In spite of a good appe- 
tite and the ingestion of abundance of food, they even go on to a 
condition of complete marasmus. The bowels become loose, attacks 
of vomiting take place, the temperature rises a little and there are hot 






THE NEURONIC DISEASES 329 

flashes that sweep over the entire body. Muscular weakness, vertigo, 
headache, various paresthesias, slight alteration of the reflexes, spinal 
tenderness, want of energy and staying qualities all indicate a pro- 
nounced condition of neurasthenia. A true motor paresis does not 
occur, though persistent paraparesis in the legs, and even a monoplegic 
and hemiplegic condition have been recorded. 

Among the trophic manifestations a muscular atrophy is exceed- 
ingly rare. The skin, however, may be pigmented somewhat, as it is 
in Addison's disease. The hair occasionally turns gray and falls out. 
Leucoderma, urticaria, local oedema, myxedematous swellings and 
pruritus are some of the occasional and distressing associated phe- 
nomena. 

Polyuria is frequent enough to be regarded as an important symp- 
tom. In rare instances it may be associated with albuminuria or 
glycosuria. As in hysteria, epilepsy and other neuroses, the micturition 
may be excessive at times. With the polyuria and hyperidrosis, a cer- 
tain degree of polydipsia is apt to be present. Amenorrhcea has not 
been so rare in my observations as the authorities state. Delayed 
menstruation has been associated with the disease in some of the young 
girls that I have seen. The relationship between the two I am unpre- 
pared to explain. It has been thought that there is some connection 
between the sexual apparatus and the thyroid gland. The latter is said 
to undergo changes at puberty and often to vary in size with each 
menstrual period. The role played by sex in exophthalmic goitre is 
due, in my opinion, not so much to the sexual organs as to the differ- 
ences in the nervous constitution. 

The respiratory function exhibits some anomalies in Graves' dis- 
ease. Paroxysmal cough and dyspnoea are not to be made light of. 
Bryson has shown that there is a lessened expansion of the chest in 
inspiration, though Patrick has found this to run pari passu with the 
weakness of the muscular apparatus. It is not therefore a characteristic 
symptom in itself. 

Complications. — The complications of exophthalmic goitre are 
numerous and must not be confused with the symptoms of the disease. 
Among the nervous troubles with which it is sometimes associated are 
the psychoses already referred to, hysteria, epilepsy, tabes, tetany, dia- 
betes, rheumatoid arthritis, Raynaud's disease and migraine. The 
osseous system has been affected, as in osteomalacia, and has combined 
with or passed into myxedema. Optic neuritis and optic atrophy are 
complications rarely seen. Enlargement of th< lymphatic glands, 
vertigo and bronzing of the skin have- been noted by several observers. 
Valvular defects of the heart are complicating rather than symptomatic 
Organic lesions of all sorts, both in and out of the nervous system. 
except that of the thyroid gland, are so exceedingly rare that the) may 
all be put down as complications or mere secondary results. 

Diagnosis. — A typical ease of Graves' disease is easily recognized. 
Typical cases, however, arc not often seen and. moreover, the physician 
is usually called upon for a diagnosis early in the disease when tin- 
symptoms are few and not well marked. It is most desirable t«» make 
the diagnosis early, as then the disease is most amenable to treatment. 



330 THE NEURONIC DISEASES 

The tachycardia may be the only symptom present when the pa- 
tient first comes under observation. If it has come on rather suddenly, 
after a severe strain or shock in a neuropathic individual, especially a 
woman with hysteroid tendencies and a neurotic ancestry, and espe- 
cially if it cannot be accounted for on any other organic or functional 
basis, a diagnosis of incipient exophthalmic goitre may be made with 
reasonable justness. The changeability, excited character and appar- 
ently causeless origin of the tachycardia are strongly suggestive of 
Graves' disease. It is less paroxysmal in its exacerbations in the latter 
than in any other neurosis. If neurasthenic symptoms of a marked 
character occur with a tachycardia that does not change after the 
patient has maintained quiet for some time, a strong suspicion of 
exophthalmic goitre should be formed. If any of the minor symptoms, 
such as a mild psychosis, local hyperidrosis, vertigo, vasomotor dis- 
turbances, trembling and muscular weakness, reveal themselves with 
this form of tachycardia, the diagnosis is all the more strengthened. 
A careful examination for, or at least an expectant anticipation of, 
enlargement of the thyroid and prominence of the eyeballs may re- 
ward the examiner with grounds for making an absolutely positive 
diagnosis. 

If only struma is present with the tachycardia it is to be remem- 
bered that ordinary goitre sometimes provokes cardiac overaction by 
pressure upon the sympathetic and vagus nerves. Ordinary goitre, 
however, occurs mostly endemically, has not a neurotic heredity be- 
hind it, is not associated with marked neurotic symptoms, appears 
gradually, grows larger and maintains its size more uniformly than 
does the goitre of Graves' disease. In ordinary goitre the exophthalmos 
is more apt to be unilateral, and the direct irritation of the sympathetic 
is shown in the marked unilateral mydriasis. 

It must be admitted that the differential diagnosis between exoph- 
thalmic goitre and ordinary goitre with pressure symptoms is some- 
times extremely difficult. In the exophthalmic goitre I have made 
the differentiation by placing the fingers well to the side, and behind, 
the tumor and experiencing a lateral pulsation or thrill. If the tumor 
is an ordinary bronchocele, throbbing from mere promixity to the 
great underlying blood vessels, there will be no lateral thrill, but the 
whole mass will pulsate forward. 

Acute iodism (Oppenheim) and cocaine intoxication (Durdufi) 
have produced a clinical picture resembling that of exophthalmic 
goitre. 

Some of the complications may lead to confusion in the diagnosis, 
but if the cardinal symptoms of Graves' neurosis be sought for, and 
if it be remembered that most of these complications have other symp- 
toms that belong only to them and not to the exophthalmic symptom- 
complex, the differential diagnosis will not be a matter of such extreme 
difficulty. 

Prognosis. — In its ordinary form the disease is essentially a 
chronic one. It lasts for years, with remissions and exacerbations. 
Though complete recovery takes place in only about one-quarter of the 
cases, and these the milder ones, death, on the other hand, need not 



THE NEURONIC DISEASES 33 1 

be feared, except in the more rapid and severe cases. Intermissions oc- 
cur in some cases, so that the patient suffers from a series of attacks. 

The light cardiac cases are the most hopeful. These sometimes 
return to health in three or four weeks. They may become chronic, 
develop other symptoms and last for years. Gowers finds that the 
prognosis in these cases is a trifle better in women than in men and 
where the disease seems to run through the family. 

With the appearance of struma and exophthalmos the prognosis 
becomes more grave. Very serious is it if the apparent cause is 
irremediable, if there is marked emaciation, if the thyroid is unusually 
enlarged and if the muscular weakness is extreme. Organic heart 
disease renders the outlook unfavorable. 

Xo case, however severe and prostrated it may be, is absolutely 
beyond all hope of restoration to health. Some very remarkable and 
unlooked-for recoveries have taken piace. In those that do recover 
the heart disturbance is apt to linger or be the last symptom to go. 
Death is dependent usually upon the cardiac weakness. Gowers .c- 
marks that the average prognosis is worse among hospital patients 
than in those of better position in private practice. My own observa- 
tion confirms this. 

Treatment. — The treatment of exophthalmic goitre is still un- 
satisfactory, whatever the means employed. Every line of treatment 
has been followed by some cures ; no line of treatment has been tried 
without a certain percentage of failures. In view of this fact, one is 
inclined at times to believe in the self-limitation of some of the cases, 
especially when we recall how remittent and even intermittent the 
disease often is in its course. Credit must not be too hastily gJvcn, 
therefore, to any particular mode of treatment that happens to be fol- 
lowed by improvement. 

The treatment of this disease may be profitably discussed under 
the five heads, specific, hygienic, medicinal, electrical and surgical. 

There is no known specific remedy that will cut the disease short. 
Recently, however, some favorable results from the exclusive adminis- 
tration of milk drawn from thyroidectomized goats have been reported 
by Ballet. Enriques, Mobius, Lanz and others. The theory is that 
animals from which the thyroid gland has been removed develop 
in their bodies a substance that would fix or neutralize the poisons 
of Graves' disease. Goebel argues that in Graves' disease, depending 
upon a hypersecretion of thyroidin, iodin is advantageously excluded 
from the dietary and this Is accomplished by the giving of milk only 
from an animal deprived of its power of secreting any iodin through 
the removal of its thyroid gland. 

The duration of this treatment varies from several weeks t<> six 
months, and has been followed by very encouraging results. 

The serum from thyroidectomized goats and sheep has been used 
by Mobius, Burghardt and Blumenthal with some degree of success. 
It is administered per <>s and subcutancously. By the latter method 
I ccm. has been injected daily, while at the same time rodagen, a 
powder prepared from the milk of thyroidectomized sheep, was given 
three times a day in dos< s of 3 to 6 grams. I !ases with organic cardiac 



3$2 THE NEURONIC DISEASES 

affections generally got worse and in some instances the serum pro- 
duced erythema, rheumatoid troubles and general depression. 

All forms of serum treatment have as yet been tried in too small 
a number of cases to be positively recommended or condemned. 

There are no prophylactic measures to be noted, as the disease 
usually makes its appearance more or less abruptly. General hygienic 
measures are of immense value when the trouble has once announced 
itself. First among these is rest and absolute quietude of mind and 
body. Removal of all sources of worry, a change of environment and 
a certain amount of rest daily in bed will cause an amelioration in the 
symptoms of nearly every case, and their disappearance completely in 
not a few of them. A sojourn, therefore, in the country where plenty 
of fresh air and good food, with quiet, can always be obtained, is 
judicious. 

The food should be plain, non-stimulating and largely vegetable. 
Alcohol, tea and coffee should be prohibited absolutely and meats 
largely restricted. 

Most patients do better at the seashore than in the mountains, 
though some have improved in high, dry altitudes. Sea-bathing and 
mountain-climbing are decidedly dangerous, as is also a sea-voyage, 
unless the patient is proof against mal dc mer. Gentle outdoor exer- 
cise and moderation in bathing are to be recommended. Sexual ex- 
citement, smoking and all forms of dissipation and unwonted mental 
and physical stimulation must be interdicted. The patient must adopt 
a most regular mode of life in regard to his sleeping, rising, eating, 
etc. Some cases do better when they keep their bed absolutely for a 
few weeks, though in the majority of cases this is not required. 

As advanced cases, in which operative measures have been sug- 
gested as a dernier ressort, have recovered when the above line of 
treatment has been rigidly and persistently carried out, too much stress 
cannot be laid upon the hygienic treatment of the disease. 

In addition to the sedative and tonic effect of these hygienic meas- 
ures, the effect of the physician's personality, the hopefulness of mind 
that can be inspired by the companions of the patient, and the remarka- 
ble influence of psychic suggestibility are important and rather favor the 
neurotic theory of the disease. It is a curious fact that Mobius, who 
first propounded the glandular theory of the disease, has reported some 
good results from the use of hypnotism. Oppenheim, who questions 
the thyroidation theory and favors the neurotic, has never seen hypno- 
tism do a particle of good. I am convinced, nevertheless, that a certain 
amount of psychic suggestibility plays a useful part in the management 
of the disease, and I am not sure that some of the vaunted cures from 
surgical as well as from other measures may not be due to profound 
mental impression. 

Tlie medicinal agents that have been employed to combat the dis- 
ease are many. Most of them are used to combat the symptoms. Suc- 
cesses and failures have followed all of them. None oi them can 
be recommended with certainty, though all of them should be given a 
trial before the ease is declared hopeless or subjected to the risk of a 
severe operation. Like all experimenters, T have my own favorite 



THE NEURONIC DISEASES 333 

remedy, though at times I have found it to fail me. I have seen codeia, 
in gradually increasing dosage, continued for a considerable time, 
produce prompt and happy amelioration of both subjective and ob- 
jective symptoms. I give th ; s alkaloid a trial in every case before re- 
sorting to other measures. Sometimes I have had better results from 
the administration of asafcetida in full doses at the same time. The 
heart action has quieted down, the struma has seemed to lessen in size, 
and above all, the patient's general nervous condition has disappeared. 
The bromides have been less effective in my hands, though beneficial in 
some cases. I have seen no results from belladonna or its alkaloid, 
atropia, such as others have reported. I have given it until the physio- 
logical effects were decided. The administration- of iodine and the 
iodides is full of. uncertainties. The symptoms are less liable to be 
increased under the use of hydriodic acid. In a few instances good 
has followed all of them and they are open to trial if watched and 
given cautiously. Painting the skin over the gland with iodine, or 
rubbing into it daily the ointment of the red iodide of mercury, is 
urged by some authorities. Iron, quinine, arsenic and the mineral acids 
serve as useful general tonics. Oppenheim urges the avoidance of 
opium for the diarrhoea and says that he has had better success with 
Colombo. For their symptomatic effect tincture of aconite, aconitia, 
strophanthus, digitalis, cactus grandiflorus, veratrum viride and picrate 
of ammonium have received various indorsement. Phosphate of 
sodium daily in doses of two to ten grains has been praised by Kocher 
and others. 

The very multiplicity and diversity of these remedies suggest their 
own criticism. They are probable useful in combating certain condi- 
tions in individual cases, but as distinct therapeutic agents for the 
cure of exophthalmic goitre they are practically worthless. They arc 
merely adjuvants in fostering the nervous quietude and bodily nutri- 
tion upon which the real cure of the disease depends. 

Before leaving the discussion of medicinal agents, a word should 
be said in regard to the administration of thyroid extract, so much 
lauded a few years ago and now so extensively condemned. It is 
true that the symptoms of the disease are usually increased by it. and 
for that reason it must be given, if given at all. with great caution. 
It is curious logic to base the thyroidation origin of the disease upon 
this fact, as many do; for as the administration of thyroid extract in 
all neuropathic individuals will provoke more or less nervous dis- 
turbance (a quarter of a grain produced a disturbing degree <>t' excite- 
ment in a case of myxoedema, and in another of sporadic cretinism 
under my observation), the increase of symptoms produced by its 
administration in Graves' disease merely indicates the neurotic origin 
of them in this affection. T have seen ;i case in a young man w I 
mother had the disease in an advanved stage, and whose brother 
showed it in its incipience, completely cured and without any dish 
ing phenomena, during its intermittent administration in five-grain 
doses during a period <■(' almost eighteen months. I do not think. 
therefore, that it is open to absolute condemnation, though I would 
urge caution, and some hesitancy, in its administration. 



334 



THE NEURONIC DISEASES 



Electrical treatment should always be given a trial, as some very- 
favorable results have followed it. Galvanization of the cervical sym- 
pathetic is the method of choice. Two or three times a day, in ten- 
minute seances, and in doses of three or four milliamperes, the stable 
current should be transmitted along the anterior edge of the sterno- 
mastoid muscle. It is a question whether the effect is upon the sym- 
pathetic or the vagus nerve. The same mode of application in health 
does not cause any pupillary changes, which seems to indicate that 
the sympathetic is not very much involved. Strong currents must not 
be used, and it is better to err on the side of too small and too brief 
an application than vice versa. The patient should lie down during the 
treatment. Dana recommends placing the positive pole beneath the ear 
and the negative over the thyroid gland for two minutes, then over the 
cardiac region one minute, positive pole over the eyes, and finally the 
negative over the thyroid one minute. Vigouroux and Charcot long 
ago recommended the direct galvanization of the cardiac region. The 
static breeze in the same area is said to have done good. General 
faradism and central galvanization are useful for their general tonic 
effect. Electrical treatment often fails, and I am prone to think that 
some of the good accomplished by it is due to psychic suggestion, ex- 
pectancy, hopefulness and the systematization of the patient's general 
regimen inculcated by it. It therefore has its use. 

One enters a battlefield in discussing the surgical treatment of 
exophthalmic goitre. Here, as elsewhere, good reports are forthcom- 
ing. All of the operations are dangerous, and the danger increases 
with the stage of the disease and the inexperience of the operator. 
Whereas so great an operator as Kocher may report a hopeful per- 
centage of cures in carefully selected cases, physicians will be loath 
to regard exophthalmic goitre as purely a surgical affection until no 
cases are cured by other measures, and until the statistics and tech- 
nique of the average surgeon make a better showing. 

This is not the place to discuss the relative merits of medical and 
surgical treatment. Many analyses will have to be scrutinized and all 
the bearings taken fully into account before the question receives any- 
thing like a definite answer. 

Five operative procedures are to-day before the medical world for 
consideration. In the order of their popularity and usefulness they 
may be enumerated about as follows: Sympathectomy, or exsection 
of the cervical sympathetic nerve ; thyroidectomy, with a mortalitv 
ranging about fifteen per cent ; ligation of the thyroid arteries ; 
Jaboulay's exothyropexie (exposure of the gland to the air) ; and 
operations upon distant organs, as, for example, the uterus. 

By operative procedures good results are claimed in from sixty 
to eighty-five per cent, of cases. The mortality is so varied in the hands 
of different operators that at present nothing definite can be affirmed. 



MYXGEDEMA VXD CRETINISM. ATTTYREA. 

Myxcedema, cretinism and cachexia strumipriva are three condi- 
tions dependent upon disease of the thyroid gland and characterized 



THE NEURONIC DISEASES 335 

by a peculiar condition of the skin and mucous membranes, by weak- 
ness and certain nervous manifestations, and by a psychosis of a more 
or less uniform and typical sort. Absence of the thyroid gland is the 
basis of the trouble, as shown both by post-mortem examination and 
by the brilliant results obtained from the administration of thyroids. 
The three diseases may therefore be well considered together, and on 
account of the prominence of their nervous symptoms be included in a 
work on nervous diseases. 

It was Sir William Gull, and later on Ord, who in the seventies 
first described a cretinoid condition in which mental failure and a 
myxedematous condition of the subcutaneous tissues were associated 
with atrophy of the thyroid gland. There were no pathological find- 
ings of any moment, though the pathogenesis of the disease was 
attributed to the loss of the thyroid gland. The suspicion was trans- 
formed into a certainty when a similar condition was produced by 
extirpation of the gland by several investigators. Horsley established 
the condition by a complete removal of the gland in monkeys, and 
Kocher and Reverdin showed that it followed complete extirpation in 
the human. This operative myxcedema, or cachexia strumipriva, is 
characterized by a tired feeling, pains and heaviness in the limbs, 
tetanoid contractures, sensations of cold, temporary swelling of the 
face, hands and feet, mental apathy and coma. A chronic state gen- 
erally follows this in which the mentality becomes sluggish, the skin 
cold, dry and scaly, and the strength decidedly diminished. The hair 
may fall out, the bones cease to grow and the patient die if not treated. 

This cachexia appears more promptly in the young than in the 
old and is believed to occur only when the gland is entirely and com- 
pletely removed. The identity of these symptoms with those of 
myxcedema in the adult and % cretinism in the child has confirmed 
pathologists in the view that the same pathogenesis is applicable to all 
these conditions. 

MYXCEDEMA. 

This is sometimes called Gull's disease. Charcot named it cachcxie 
pachydermique. It has been referred to as cretinism in the adult. 
The disease comes on insidiously and progresses slowly. Women are 
more affected than men in the proportion of six to one. It occurs 
mostly between the ages of thirty and fifty. It has been seen in in- 
fants, but not earlier than at six months of age. There is a slight 
hereditary influence on the maternal side, and several eases have ap- 
peared at times in the same family. Other neuroses have preceded it 
and exophthalmic goitre has been replaced by it. Alcoholism and 
syphilis do not predispose to it. Though it occurs so largely in women, 
the sexual accidents of women do not seem to have any bearing. 

Various exciting causes have he en assigned, such as exposure' to 
cold, emotional excitement, traumata, etc. 

Symptoms. — Trophic changes constitute the main symptoms in 
the clinical picture. There is a slow and gradual increase in the 
general bulk of the body. The head and extremities enlarge, assume 
a new contour and take on a new shape. The countenance especially 



336 THE NEURONIC DISEASES 

appears swollen and puffy. The lines of expression are obliterated, the 
lips thickened, the nostrils broadened^ the mouth enlarged and the 
entire features rendered coarse and brutal. Apathy and stupidity are 
suggested by the physiognomy. The tongue is thickened and hard- 
ened. Local swellings occur in the neck and on the extremities. The 
tumefaction, especially in the supra-clavicular region, includes the skin 
and subcutaneous tissues. The hands and feet are stubby, the fingers 
and toes broad and separated. The skin is dry, hard and scaly, is 
rough and does not pit upon pressure as in ordinary oedema. It feels 
cold and dead, looks pale, seems elastic to the touch and does not 
perspire. The mucous membrane of the mouth is also infiltrated. 
Imperfect nutrition is shown in the falling out of the hair, nails and 
teeth. Muscular weakness and mental deterioration added to the 
physical deformity render these individuals awkward, ungainly and 
clumsy in all their movements. 

The psychic condition is the second important characteristic of 
this disease. There is a gradual impairment of the mental faculties. 
The thoughts and perceptions are slow, the speech is delayed and the 
general intelligence greatly lowered. At first the memory is weakened. 
The disposition becomes irritable and suspicious. Hallucinations and 
delusions that are inconstant and systematized, and suicidal impulses 
may all be observed. Sometimes there is merely inability to fix the 
attention and lack of mental energy. At other times there is a total 
lack of interest and a settled state of stupor. Finally a condition of 
complete dementia obtains, in which there seems to be an obstruction 
in all the avenues of both afferent and efferent impulses. The five 
senses are all more or less impaired. At times there is great depression 
and despair, which, however, is not identical with true melancholia. 
Mania, melancholia and hallucinatory paranoia have been observed. 
This group of mental symptoms differs in its course from those of the 
ordinary psychoses and is as typical in its general characteristics of 
myxcedema as are the physical signs. 

Headache, vertigo and coldness are often complained of by these 
patients. The bodily temperature is not unfrequently found to be sub- 
normal to the extent of one or two degrees Fahrenheit. The muscles 
are weak and sometimes atrophied. Incoordination and contractures 
are observed in rare instances. The electrical resistance of the skin 
is increased and it is often hypaesthetic or even anaesthetic. The voice 
is unnatural, hoarse and monotonous. The reflexes, the electrical re- 
action of the nerves and muscles, the functions of the abdominal and 
thoracic viscera are all normal. Hemorrhages are not infrequent. 
Albuminuria is observed in about twenty per cent, of the cases; gly- 
cosuria rarely. Synovitis of the knee-joint, optic neuritis and optic 
atrophy are among the rarest symptoms that have been noted. 

The physical deformity, the peculiar infiltration of the skin and 
subcutaneous tissues, the tncnlalization, the hoarse voice, the weakness 
and awkwardness are so characteristic a group of symptoms that the 
diagnosis of myxedema is never a very difficult matter. Were any 
doubt present, the therapeutic test with thyroid extract would soon 
remove it. 



THE NEURONIC DISEASES 337 

The course of the disease is chronic and progressive, often ex- 
tending over five, ten and fifteen years. 

The prognosis without treatment is unfavorable ; with treatment 
it is extremely bright, so far as complete or partial restoration to a 
normal condition is concerned. The treatment, however, has to be 
■continuous, as its cessation is usually followed by a prompt relapse. 
When death occurs it is usually the result of some cardiac trouble or 
.some intercurrent malady, such as tuberculosis. 

In view of the accepted pathogenesis of myxcedema, it is hard to 
explain those cases in which exophthalmic goitre is associated with it, 
as well as those in which an enlargement of the thyroid in young per- 
sons gives rise to an acute and temporary manifestation of it. I have 
seen it follow exophthalmic goitre, but this is not so difficult to ac- 
count for. 

Probably in all these conditions there is an enlargement of the 
thyroid generally with complete atrophy of its parenchymatous, secret- 
ing structures. 

CRETIXISM. 

This is a form of myxcedema occurring endemically and sporadi- 
cally, appearing congenitally or during infancy, having the same gen- 
eral symptoms as the adult form, and depending upon disease or ab- 
sence of the thyroid gland. Endemic cretinism occurs chiefly in 
Switzerland, Italy and France and is associated with goitre. It is 
"believed to be due to the loss of function in the thyroid gland. 

Sporadic cretinism is rare, especially in this country, and is in all 
respects identical with infantile myxcedema. Cases of so-called 
infantilism are probably mild grades of the same condition. 

Rarely before the age of six or seven months is the disease rec- 
ognized. Then the same general trophic and mental deterioration is 
noted. The growth and mentality of the child are seen to be retarded. 
The face assumes a bloated, coarse, stupid appearance. The tongue 
is large, the lips protuberant, the mouth increased in size, the eyelids 
thick and drooping and the facial lines obliterated. The body is 
dwarfed and thick, the abdomen pendulous, the extremities short, club- 
shaped and bowed. The hands and feet resemble paws. Hair is scarce, 
the teeth are undeveloped or decayed, the nails are deformed or absent. 
The skin is pale, sallow and waxy ; it is dry and leathery to the touch. 
Fatty tumors abound in and about the neck. The disproportion be- 
tween the various parts of the body is very remarkable. The mind fails 
of development and a condition of idiocy thus obtains. The muscula- 
ture is weak so that the child has to be supported when walking. Usu- 
ally walking, like speaking, is quite impossible. The fontanelles com- 
monly remain unclosed. 

There are mild degrees of the trouble in which the physical symp- 
toms are only slightly indicative of delayed development and the 
mental state is that of medium grade imbecility. Such a ease I have 
seen restored almost to a normal condition by the administration of 
thyroid extract. The thyroid gland is supposed to be affected by a 
transient functional disturbance. 



338 



THE NEURONIC DISEASES 





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V 

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u 







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THE NEURONIC DISEASES 339 

Death occurs early in most cretins, though some have lived to 
middle adult life. If treatment is instituted early and before puberty, 
or the age at which puberty should occur, most brilliant results in 
some cases may be obtained. 

Treatment. — There is only one remedy that is effective in all 
these forms of athyrea or alhyreosis, and that is the thyroid gland or 
thyroid extract. We are originally indebted to Murray for this remark- 
ably brilliant therapy, though much has been done in the way of es- 
tablishing it by Schiff, Bercher, Horsley, MacKenzie, Horwitz and 
others. 

Beginning with one grain three times a day, the dose may be 
continuously increased until fifteen or twenty grains three times a day 
are taken. Forty grains or more is about the maximum average daily 
dose. 

Unpleasant symptoms that are to be guarded against are those of 
general thyroidism — namely, paresthesia, restlessness, tachycardia, 
dyspnoea, anorexia, emaciation, delirium, etc. These occur, however, 
in only a small number of cases. On the other hand, the results of 
thyroid treatment are so positive and happy that nothing in the way of 
therapeutical success can compare with it. 

Relapses occur if the remedy is discontinued ; hence, as Murray 
himself suggested, full doses should be given at first to effect the cure 
and moderate doses should be continuously administered thereafter 
to maintain the normal or acquired metabolism. 

Thyroidin, thyroiodin, idiothyrin have all been prepared from the 
thyroid glands of sheep and tried in place of the thyroid extract. 
While some advantages are claimed for them, especially the iodothyrin, 
none of them equal in efficiency the whole gland or its extract. 

ACROMEGALY. 

As Marie first described this disease in 1886, it is sometimes named 
after him. It has also been called Pachyakria. As its more common 
name indicates, it is chiefly characterized by an enlargement of the ex- 
tremities and face. 

Etiology. — Heredity seems to exercise no influence in its etiology. 
All ages are liable to it, though the great majority of cases occur 
between twenty and forty. Most authors declare that it attacks both 
sexes about equally, though I am inclined to think that women are a 
little more prone to it than men. Race and nationality exert no deter- 
mining force. It has followed syphilis, rheumatism, the infectious 
fevers and alcoholism, though it is doubtful if these are in any way 
causative. Such recorded exciting causes as exposure to cold, fright, 
worry, emotional shocks and traumata are too indefinite to be given 
much consideration. 

Pathology and Pathogenesis. — The mosl constant post-mortem 
finding is enlargement of the pituitary gland (cerebral hypophysis). 
In practically every case this is found to be altered. The other findings 
in the disease are comparatively so inconstant the opinion has become 
quite universal that the primary seat of the trouble resides in this gland. 



340 THE NEURONIC DISEASES 

Those who question this hypothesis base their opposition upon the fact 
that often the hypophysis is diseased without the appearance of the 
acromegalic symptoms.. Various neoplastic growths, such as sarcoma, 
glioma, adenoma, have been found as the reason of the pituitary en- 
largement, especially of the anterior part of the gland. The function 
of the gland is disturbed and a general nutritive disorder is thus estab- 
lished. The exact function is not positively known, though embryol- 
ogy,, evolution and pathology all seem to indicate that it bears a close 
resemblance to that of the thymus and thyroid glands. 

Many symptoms of acromegaly are comparable to those of 
myxoedema, especially in their tropho-neurotic characteristics. Evolu- 
tion, embryology and histology all teach that before the closure of the 
post-pharyngeal vault there was a direct connection between the mouth 
and ventricles of the brain by way of the infundibulum. The anterior 
part of the pituitary gland, having been caught in the intracranial 
cavity when the latter finally separated from the buccal cavity, its 
structures retained their thyroid-like metabolic functions, the whole 
gland became ductless and entered upon the role of an organ of internal 
secretion, and so in some way assisted in regulating the general nutri- 
tion of the body. 

In many cases of acromegaly, besides disease of the hypophysis, 
the thyroids are found to be atrophied and the thymus gland persistent 
and hyperplastic. 

The trophic changes found in other parts of the body include thick- 
ening and deformity of the bones, especially the lower jaw and distal 
bones of the extremities; arthritic conditions in and about the joints; 
hypertrophy of the skin, connective tissues, arteries and nerve-sheaths, 
spinal ganglia and sympathetic ; increase in the size of the brain, eye- 
balls and abdominal organs ; and asymmetrical degeneration of the 
posterior columns of the cord. From the pathological findings the dis- 
ease is well classified as a tropho-neurosis, whatever may be the seat 
of the primary trouble. 

Symptoms. — The disease approaches insidiously so that often the 
enlargement is first noticed by the patient's tailor or bootmaker. There 
may be at the commencement various paresthesia?, slight drawing 
pains, general debility and peculiar visual phenomena. In women 
the menstruation sometimes ceases. A persistent headache, vertigo, 
gradual failure of vision and other signs suggestive of intracranial 
tumor may awaken suspicion. Ere long, however, the characteristic 
symptom of the disease makes its appearance. This consists of a 
uniform, progressive enlargement of the hands and feet and certain 
parts of the head and spinal column. In the hands and feet the soft 
tissues, as well as the bones, are increased in size. The fingers and 
toes are not deformed, though they are big, uncouth and easily mov- 
able. They look like links of sausage. The skin is thick, but, unlike 
that of myxoedema, it is soft, moist and pliable. This enlargement 
rarely extends above the wrist or ankle. 

The same excessive development attacks the lower jaw so that a 
condition of marked prognathism is presented. The maxilla may pro- 
ject so far forward as to almost seem to encompass the upper jaw. 



THE NEURONIC DISEASES 



341 



The nose, lips and ears are enlarged. The whole face, especially 
the lower part of it, is both lengthened and widened. The cheek-bones 
are prominent. The eyelids are thickened and in some cases the tongue 
is excessive in size. 

While the long bones of the arms and legs, the metacarpal and 

FIGURE 51. 




Acromegaly. (After Marie.) 



metatarsal bones usually escape, the clavicles, sternum, ribs, patella and 
vertebral column are implicated. Kyphosis of the upper dorsal region 
is a very frequent symptom. The en si form process of the sternum is 
particularly prominent and the manubrium is so thickened that a per- 
cussion note sounds dull (Erb). The abdomen is enlarged. The skin 
under all these circumstances may continue i<> appear perfectly normal. 
As a patient of mine once expressed it. except for Ins failing eyesight 
and general change of shape, he couldn't sec that he was in any way 



34-2 THE NEURONIC DISEASES 

abnormal. In rare cases the heart is enlarged ; the penis increased in 
size ; the testicles atrophied. 

Eye symptoms are not infrequent and on account of their early 
appearance are often of extreme importance. Progressive loss of vision 
from optic atrophy is the more common trouble. All signs of irrita- 
tion, compression and destruction of the optic nerves and chiasma may 
be expected. Optic neuritis is much rarer than optic atrophy. Hemi- 
anopsia of various types, hemiachromatopsia, unilateral blindness with 
hemianopsia in the other eye, are some of the more common visual 
disturbances. 

Fig. 52 portrays the visual fields of a patient of mine before he 
went totally blind. For a time he had horizontal hemianopsia, so 
that everything below the level of his eyes was invisible. This lasted 
about six months and gradually passed into the bitemporal type shown 
in the chart. 

The ocular muscles are sometimes paralyzed with transient or 
permanent attacks of diplopia. Flemianopic pupillary rigidity may be 
present. Exophthalmos has been observed, but is exceedingly rare. 
Pressure by the enlarging hypophysis explains easily these various 
transient and permanent ocular manifestations. 

The mental state of these patients is always somewhat affected, 
though not so characteristically as it is in myxcedema. They are 
apathetic, sluggish and devoid of energy. A sort of a drowsy air and 
heaviness belongs to them. Their movements are slow and awkward. 
There is a weakness of their muscles, though their electrical reactions 
are unaltered. The condition of the reflexes varies, but is of no special 
import. 

There are many other symptoms that may appear, but are not 
constant enough to be considered typical of the disease. Some of 
them are merely indicative of an intracranial new growth ; others are 
partly due to the disease itself and partly due to associated derange- 
ments. The thyroid may be enlarged, more commonly it is diminished 
in size. The skin may be thickened, but it is never myxcedemafous. 
The muscles are sometimes wasted. The larynx may be altered in 
shape and the voice rendered deep and rough. Its mucous membrane, 
like that of the mouth, is thickened. All of the five senses may be 
blunted. With the enlargement of the heart the pulse rate may be 
accelerated. Impotence is usually present. Sweats sometimes occur, 
along with polyuria and polydipsia. Bulimia or polyphagia is rather 
frequent. Pigmentation, moles, warts, keloids, fibromata and neu- 
romata are often observed. Dyspnoea, palpitation, vasomotor neurosis, 
general weakness and mental depression are not to be unexpected. 
Epileptic attacks have been recorded in rare instances. 

Diagnosis. — The diagnosis depends upon the onset of the disease, 
the peculiar enlargement of the lower part of the face and extremities. 
the kyphosis, the ocular symptoms and the mentality. 

Myxcedema and cretinism are to he differentiated by the limitation 
of the enlargement to the soft tissues, the infiltration of the subcutane- 
ous structures of the entire face, hands and feet, the cold, harsh, (In- 
state of the skin, the alopecia and the dementia. The hones are not 



THE NEURONIC DISEASES 



343 



hypertrophied as they are in acromegaly, ncr are the kyphosis and 
prognathism present. 

Gigantism is closely related to acromegaly, if it is not identified 
with it. Many giants become acromegalics. Massalongo. Klebs, Meige 
and others believe that the primary disease in both conditions resides in 
the hypophysis cerebri. 

Partial gigantism or hypertrophy of special parts of the body 
(hemihypertrophy, macropodia. macrocheiria, etc.) is a congenital 
trouble and is distinguished from acromegaly by its limitation to a 
particular part of the body and the great deformity of that part. 

Syringomyelia, adoposis dolorosa, elephantiasis, leontiasis ossea. 
diffuse hyperostosis, osteitis deformans have all their own characteristic 



FIGURE 52. 




Bitemporal hemianopsia in a case of acromegaly in which complete blind- 
ness ultimately occurred. Implication of the optic chiasm is clearly shown in the 
perimetric fields taken by Dodd. An autopsy being denied, I assumed from the 
history and other features of ;hc case that the hypophysis was the seat of a 
sarcoma. 

symptoms and can be distinguished from acromegaly by a close study 
of the total clinical picture of the latter. 

In osteitis deformans. Paget's disease, the shafts of the long bones 
and the bones of the cranium, not those of the face, are enlarge. 1 and 
softened. The long bones are curved from the weight upon them. 
Pains are present in them almost constantly. There seems to be a 
close relationship between this affection and malignant tumors. Noth- 
ing is known of its etiology and its treatment is without results. 

Leontiasis ossea is characterized by a hyperostosis of the cranial 
bones, sometimes also of the face. The head, face and neck, with both 
the hard and soft tissues, increase slowly and | vely. Stan- 

has named the condition megalocephaly. 

M acromegaly is curious as the antithesis of acromegaly. It was 
described bv Hutchinson and Gilford in [896. There is a defect 01 



344 



THE NEURONIC DISEASES 



FIGURE 53. 




Pulmonary osteoarthropathy of Mario. 
(From a photograph in the Pathological Museum of the Mod. Dcpt. of the 
University of Illinois.) 



THE NEURONIC DISEASES 345 

nutrition, due to some form of nervous trouble, which is seen In the 
smallness and immaturity in some parts and consequently a relative 
largeness and apparent prematurity in others. 

Marie's hypertrophic osteo -arthropathy, which occurs in associa- 
tion with cardiac and pulmonary disorders, deserves special attention 
in the differential diagnosis of acromegaly. In this disease the bones 
are more involved even than they are in acromegaly. Arnold refers 
to the disease as a secondary hypertrophic osteitis. In this disease 
prognathism is not present and kyphosis, if at all present, is lower down 
in the spinal column. The end phalanges are peculiarly deformed, the 
wrist and ankle-bones are enlarged and the finger tips are club-shaped. 
There is no uniformity in the enlargements. Moreover, the tongue is 
not affected as it is in acromegaly, and the mind is clearer. 

Prognosis. — Sternberg notes three varieties of the disease in 
regard to its course. The first is benign and may last fifty yeais; 
the second is the usual chronic form and may continue from eight to. 
thirty years ; the third is the acute, malignant form that terminates 
in about three or four years. The disease is incurable, but at times it 
ceases to progress. Relapses occur. Death is usually the result of 
marasmus, diabetes, heart disease or some intercurrent trouble, such as 
cerebral tumor, bedsores, secondary disease of the genito-urinary tract. 

Treatment. — Treatment is unsatisfactory. Organotherapy has 
so far proved to be entirely ineffective. Thyroid and pituitary extracts 
have been administered without results. It has been reported that the 
iodides, mercury and arsenic have seemed to have arrested the disease 
— an open question always where the disease is prone to cease 
progressing of itself at times. The attempts of Caton and Paul to 
bring about a cure by extirpating the pituitary gland are not very en- 
couraging. Symptomatic treatment is about all that we can offer the 
victims of this disease at the present time. 

ADIPOSIS DOLOROSA. 

This is sometimes called Dercum's disease, because it was first de- 
scribed by Dercum in 1888. A considerable number of cases have 
been described since and even examined post-mortem. 

The appearance of painful, fatty tumors just beneath tlie skin in 
various parts of the body is its cardinal clinical manifestation. Changes 
in the thyroid and pituitary bodies, and a neuritic condition in the 
peripheral nerves, are its chief pathological findings. 

The disease usually appears in persons of a nervous temperament 
in the middle period of life. The majority of the cases have been 
over forty years of age. The women are often hysterical, and both 
men and women are highly susceptible to suggestion. A general 
asthenic and neuropathic condition usually characterizes them. 

The pathology and pathogenesis of the disease are not clear. The 
three prominent findings ire the fatty tumors, the neuritis and the 
changes in the thyroid gland. 

The fatty tumors occur anywhere on the body jusl beneath the 
skin, are variable in size and in no way differ from ail lipomata. hi 



346 



THE NEURONIC DISEASES 



the tumors the nerves seem to be increased in number and are in a 
condition of interstitial inflammation. 

The thyroid gland exhibits a state of cystic degeneration with 
partial atrophy and the acini filled with colloid material. 

Adiposis dolorosa is clearly a tropho-neurosis, but where the pri- 
mary source of the trouble is to be looked for we can no more deter- 
mine here than we can in any other tropho-neurosis. As Billings has 
said, it is as yet only an interesting clinical entity. Its classification 
must await further knowledge in regard to the pathogenesis of this 
disease as well as other tropho-neuroses, like acromegaly. 

No treatment of the trouble has been of any avail in checking the 
formation of the tumors. A few cases have been reduced in weight, 
the asthenia and mental depression removed, and the internal meta- 
bolism apparently placed on a somewhat better basis by the adminis- 
tration of thyroid extract. 

SCLERODERMA. 

This remarkable disease is believed by most authorities to-day to 
be a tropho-neurosis. 

The chief feature of it is a localized or diffuse induration of the 
skin. 

Etiology. — Females are attacked by it far more frequently than 
males. Kaposi afhrms that seventy-five per cent, of all cases are women. 
The middle period of life is the time of its appearance generally. Osier 
believes that it is more frequent in this country than statistics would 
seem to indicate. Its immediate cause is unknown. Some believe the 
disease is a tropho-neurosis of spinal or sympathetic nerve origin. It 
certainly seems to be closely related to progressive facial hemiatrophy, 
and it is not unfrequently associated with Raynaud's disease, erythro- 
melalgia, Addison's disease, rheumatic troubles and exophthalmic 
goitre. 

Others still continue to regard it as a true skin disease, due to 
some local affection. The old view that it was due to closure of the 
thoracic duct or other lymphatics and a stagnation of the lymph has 
not been confirmed by the more recent examinations. 

Pathology and Pathogenesis. — Beyond the obvious symp- 
tomatic changes, the pathological findings are not of special significance. 
The changes in the skin, the connective tissue over-growth, the disap- 
pearance of the subcutaneous fat, the increase of elastic fibers, have 
given the name to the disease. The vessels are numerous, but dimin- 
ished in calibre. 

The entire affection is in all likelihood a primary, connective- 
tissue hypertrophy of nervous origin or disturbance, ending in resolu- 
tion or atrophy. The neurotic nature of the disease is strongly sug- 
gested by numerous observations. Schwimmer's cases revealed disease 
of the peripheral nerves. Westphal saw significant changes in the 
brain. Eulenberg and others have reported the association of pro- 
gressive facial hemiatrophy and other tropho-neuroses with the disease. 
In some cases marked arthritic changes have been observed not unlike 
those seen in the Charcot joint. 



THE NEURONIC DISEASES 347 

Symptoms. — In exceptional cases these begin with chills, fever and 
other signs of inflammation. More generally, however, the first symp- 
tom noticed is the growing stiffness and rigidity of some portion of the 
skin. This slowly increases during months and years. It is most 
noticeable and often limited to the upper extremity, though it may 
appear in the lower. It may occur in circumscribed patches or be 
diffused over a very large area. Sometimes the spots are disseminated 
at first and later on run together. The face and neck are not unfre- 
ouently involved. The trouble is usually bilateral, but is sometimes 
unilateral. The lips may be retracted or the gums exposed. The 
nose may be greatly attenuated, giving the physiognomy a very dis- 
agreeable appearance. The hands are tense and glossy, the fingers 
thinned and club-shaped and the metacarpophalangeal articulations 
.sometimes subluxated. As the subcutaneous fat atrophies the skin 
•clasps the bone and reveals sharply its outlines. 

The diseased skin is cold, thick, rigid and hard. It feels like the 
derma of a frozen corpse. It is not sharply delimited from the normal 
skin, though it often has a hypersemic tract around it. It is swollen 
in the neighborhood or shrunken. The surface of the epiderma is 
smooth, shining, scaly, whitish in color or pigmented in patches. In 
the beginning it is often merely (Edematous and hypertrophic. 

The mucous membrane of the mouth and vagina often exhibit 
similar alterations. 

Wrinkling, of course, ceases, and all actions implicating the »*m, 
like laughing, winking, breathing, become difficult and impeded. The 
muscles beneath are usually indurated, shriveled and atrophied. The 
bones are thinned. Peculiar constrictions, mutilations, even spon- 
taneous amputations and ulcerations have all been seen. Sclerodactyly 
or characteristic crippling of the fingers occurs. 

The sensibility is rarely involved, though it may be somewhat 
blunted. The tenseness is felt by the patient and sometimes pain, itch- 
ing or paresthesia. Paralytic symptoms occasionally appear. Hypo- 
chondriacal neurasthenia usually exists. There is general marasmus 
and the patient is depressed mentally. In some instances amyloid de- 
generation has been found post-mortem in the lungs, heart and 
kidneys. 

Besides the diseases mentioned under the head ^i etiology, sclero- 
derma has been complicated by eczema, acne, erysipelas, herpes zoster, 
variola, morphoea and keloid. Its diagnosis is not difficult. 

Prognosis. — Rarely the disease disappears by involution. The 
retrogression is gradual, often only in spots The trouble is always 
a chronic one, with remissions now and then during its long course. 
Most cases go on to the formation of ulcerations, mortification and 
other complicating conditions, suffering all the while with pains, insom- 
nia, bad nutrition, and finally die from marasmus. 

Treatment.— There is no known cure for scleroderma. Nutri- 
tion, rest, good general hygiene and such general tonics as iron, qui- 
nine, arsenic and cod-liver oil are m order in all cases. Salol internally 
in fifteen-grain doses three times a day has seemed to have been bene- 
ficial in a few instances. Improvement has occurred in many c 



34^ THE NEURONIC DISEASES 

under thyroid medication. Galvanization of the sympathetic was 
urged by Schwimmer, and the local application recommended by Pif- 
fard, Fieber and others. 

Ointments and local medication are frequently grateful. Xaphthol. 
salicylate ointment, mercurial and iodine soaps and preparations, and 
copper oleate are thus available. To these should be added local baths 
and massage. 

PROGRESSIVE FACIAL HEMIATROPHY. 

This is a very rare affection in which one side of the face under- 
goes a remarkable progressive wasting, and is probably due to a dis- 
turbance of the trophic functions of the trigeminal nerve. The earliest 
accounts of it were given by Parry and Romberg. 

Etiology. — Little is known of its causation. It prevails more 
among women than among men. It is first recognized in early adult 
years, though it usually starts in childhood and in many cases seems 
to be congenital in origin. Being a chronic, progressive disease, it may 
run on into old age, but it is rarely ever seen to start after thirty. 
It has followed slight injuries to the face and head, acute rheumatism,, 
scarlatina, diphtheria and typhoid fever. It is not known whether the 
neuralgic pains in the fifth nerve that sometimes accompany it early in 
its course bear a causal or symptomatic relationship to it. A general 
inherited neuropathic taint has been detected in some cases. 

Pathology and Pathogenesis. — The only pathological findings 
that are of any significance are those which enter into the symptomatol- 
ogy of the disease. 

The pathogenesis of the disease is almost wholly conjectural. I 
am inclined to follow Gowers' view that it is an organic affection of the 
fifth nerve or its Gasserian ganglion. The marked limitation of the 
symptoms to the peripheral area innervated by this nerve is only ex- 
plainable on this basis. The trophic character of the predominant 
symptoms and the implication of both the sensory and trophic branches 
of the nerve point to the ganglion as the primary seat of the trouble. 
Its connection with slight injuries and local infective processes are 
highly suggestive of the nature of the disease process. 

Most authors regard the trouble as primarily a trophoneurosis. 
Those who try to class the disease with exophthalmic goitre and 
migraine are illogical. In some respects it resembles scleroderma and 
yet there is not that sharp trigeminal distribution of the manifestations 
in scleroderma that there is in this disease. Moreover scleroderma 
never follows trigeminal disease under any circumstances so far as we 
know. It is a more general trophoneurosis. 

Oppenheim leans toward the sympathetic hypothesis. Bitot thinks 
it is a primary skin disease. Mobius regards it entirely as an infec- 
tive process following some local injury or sore in the neighborhood. 

Symptoms. — The symptom of the disease is described in its name, 
progressive facial hemiatrophy. Gradually there is a diminution in the 
general bulk of one side of the face. In this all the tissues partake, 
the skin, the subcutaneous elements, the muscles and even the bones. 



THE NEURONIC DISEASES 349 

The skin tightens down and clasps the bones so as to emphasize their 
outlines. The hairs fall of! and the sebaceous glands shrivel up. The 
cartilages of the nose waste causing it to be grossly distorted. The 
lips diminish on one side and are sunken. The perspiration may be 
excessive while the local temperature remains normal. The bones 
are decidedly smaller on the affected side. One side of the face is full 
and youthful, the other worn, haggard and aged looking. 

The strange physiognomy thus presented, a sort of double indi- 
vidual as it were, is so striking that the diagnosis can be made at a 
glance. The palate and tongue are usually unaffected. Sometimes, 
however, they also have been wasted on the same side. 

Xot in all cases are the muscles implicated, though the frequent 
paresis of the pteragoids, masseter, temporal, and the fibrillation and 
tremor in them, point to implication of the motor root. The electrical 
reactions are usually preserved, thus distinguishing the disease from a 
true progressive myopathy. 

Sensibility as a rule is unaffected though in some cases intense 
neuralgic pains occur early and anaesthesia or at least hypaesthesia 
later. The arteries and veins do not seem to vary in size. The saliva 
and tears are permitted to flow as usual. Tlie organs of special sense 
seem to be undisturbed so far as their functions are concerned. Bilat- 
eral atrophy has been seen occasionally and once atrophy of the skin 
and subcutaneous tissue in the back and arm of the same side was 
seen. 

The disease progresses steadily for a number of years and then 
remains stationary for the rest of life. 

Oppenheim notes the occurrences of the disease repeatedly with 
neuralgia, epilepsy and the psychoses, with chorea, spasm of the mus- 
cles of the face, jaw and tongue, once each with tabes, syringomyelia 
and disseminated sclerosis. 

The diagiwsis must be differentiated from congenital inequality 
between the two sides of the face, from facial atrophy in anterior 
poliomyelitis, and in hemiplegia of children and adults. Tt must be 
kept clearly apart from acquired facial hemihypertrophy, as describe 1 
by Montgomery, which by contrast may lead to a diagnosis of hemia- 
trr phy of the other side. And it should be distinguished carefully from 
scleroderma anVl morphcea. If it is to be regarded as a result of trige- 
minal neuritis, according to Mendel's findings, then it should also be 
carefully differentiated from atrophy due to nuclear lesions and to 
sympathetic nerve paralysis 

The gross diagnosis is easy. The minute differential diagnosis 
is sometimes rendered confusing because we are ignorant of the exact 
pathology of the disease and its limitations. Some authorities un- 
doubtedly include more in progressive facial hemiatrophy than oth- 
ers do. 

Prognosis. — Favorable as to life. Bad as to recovery. The dis- 
ease is chronic and progressive but usually becomes stationary after :t 
number of vears. The pain> are sometimes wearing and tlie limita- 
tion of movements in the muscles of mastication is sometimes annoy- 



350 THE NEURONIC DISEASES 

ing ; otherwise the patients are sound and well and suffer no very great 
discomfort. 

Treatment. — It is not amenable to any known form of treatment. 

AINHUM. 

This is a disease of the negro and is probably a trophoneurosis*. 
It was first described by Silva Lima, of Bahia, but cases have been re- 
ported by Hornaday and Pittmann, Duhring, Shepherd, and Morrison. 
It is rare in this country but has been frequently seen in South Amer- 
ica and somewhat in Asia. Its cause is not known. There is a singu- 
lar constriction o>f the skin formed about the base of one or more toes. 
Finally a deep furrow completely encircles the member, the bloodves- 
sels are obliterated and amputation takes place. The little toe seems 
to be the favorite victim. It is a chronic trouble and the toe does not 
drop off often for years. There is no sign of inflammation and usually 
no pain is connected with it. 

ORGANIC NEURONIC DISEASES. 

THE SYSTEM DISEASES. 

THE NATURE OF THE SYSTEM DISEASES AND THEIR 

CLASSIFICATION. 

In the preceding chapters the neuroses and psychoneuroses have 
been discussed. As commonly accepted, these are functional derange- 
ments of the neurones or functionating part of the nervous system. 
Our present means of scientific research is not such as to enable us 
to declare positively what the nature of the change is in the neurones 
or in their relationship to one another whereby the alteration of func- 
tion, upon which we call the condition one of disease, is brought 
about. And yet in regard to these neuroses and psychoneuroses, cer- 
tain facts stand out with a most suggestive prominence and upon these 
facts we can at least frame a working hypothesis. » 

In the first place it is to be noted that heredity, toxcemia, shock, 
strain, malnutrition and overexertion play the greatest role in their 
etiology. These causes are of a general nature and presumably act 
upon all parts of the nervous apparatus in the same way. Every 
neurone is subjected to the same deleterious influence. The nervous 
system is usually the victim in toto. 

Another fact that stands prominently forth is that no changes of 
any sort, whereupon the symptoms of these diseases can be explained, 
have ever been seen in the nervous elements. We have to assume that 
the primary trouble is inherent in the neurones themselves and entirely 
beyond our ken. It is born and has its expression there. While we 
cannot say what this inherent trouble is. we can very definitely declare 
that it involves the two primary functions of the neurones concerned. 



THE NEURONIC DISEASES 35 1 

namely, their power of exhibiting ncurility and their power of main- 
taining their own nutrition. In the very nature of things the former 
function is dependent upon the latter. 

When a neurone functionates abnormally, it is mere truism to sav 
that its power of exhibiting sensibility is disturbed. "Whether this is 
always due to a disturbance of its power of maintaining its own nutri- 
tion, as it undoubtedly is in a large number of diseases, or whether 
shock, toxaemia, strain, etc., can directly cause it to act thus abnor- 
mally without affecting in the least its power of self -nutrition, seems 
to be a debatable question. 

Change of neurility without change of nutrition or structure would 
indeed be a true functional disease. It could hardly continue long, it 
seems to me, without some structural effect being produced upon the 
intimate physio-chemical constituents of the neurone. So intimately 
related are the neural and nutritional functions of each individual 
neurone, that it is all but inconceivable that one should long be changed 
without some change in the other. 

Underlying all functional diseases, I take it therefore, there is 
sooner or later some undiscoverable but structural change. The change 
may continue to be undiscoverable and the trouble continue to be 
spoken of as functional. 

There are changes in the neurones in some diseases, however, that 
are observable under our present staining and microscopic methods of 
examination. We speak of these as degenerative changes. Even- 
neurone in the body is liable to them and all parts of the neurone, cell 
and process, may be implicated. 

There are all degrees of degeneration from that which is scarcely 
detectable down to the complete atrophy and disappearance of the en- 
tire neurone. 

Every indication points toward the fact that the degeneration is 
a nutritive change and that it is dependent upon the failure of the 
nutritional function of the cell-body. This is called primary deg 
emtio n. 

When any part of a neurone is severed from its cell-body, com- 
pletely or partially, that part immediately begins to undergo degen- 
eration. If the separation is complete, it will disappear entirely. This 
is termed secondary, or Wallerian, degeneration. 

Two facts are obvious, therefore, in regard to all neuronic degen- 
eration, namely, that though the process be practically identical in both 
the primary and the secondary forms, in the former it is caused imme- 
diately by an inherent functional nutritive disorder within the cell 
bodies themselves, and in the latter by the gross separation of the de- 
generating parts from their centers of nutrition. 

The distinction is an important one. The primary forms arc thus 
the result of a profound neuronic deficiency. In accordance with all 
clinical evidence, this is largely due to hereditary, toxaemic, shock, 
exhaustion and straining influences just as the functional deficiencies 
in the neuroses are. only more so. En thesi the vigor of the 

cause or the limited resistance of the neurone constituents is such that 
the mal-nutritive process emerges from its obscurity and reach* 



352 THE NEURONIC DISEASES 

stage where we can observe it with our microscope and other aids. 
When it has reached this stage — a stage, remember, which does not 
indicate the beginning or the end of a new process, but merely the 
limit of our powers of detection — we term the degeneration organic. 

A primary organic degeneration then is merely a gross, observ- 
able deterioration of the neurone resulting from a profound disturbance, 
inherited or acquired, in the nutritive function of the cell-body of the 
neurone. This would make it appear, therefore, that primary organic 
degenerative neuronic diseases are in close relationship to the neuroses. 
Perhaps the better way to state it would be that the neuroses are at 
the beginning of the organic neuronic primary degenerations or are 
earlier forms of organic troubles. 

As everybody knows the earliest clinical manifestations of all de- 
generative diseases are functional or neurosis-like in character. This 
is so common an observation that it needs but to be stated to be readily 
acknowledged. It is the reason for most of the diagnostic mistakes 
that are made in the earliest stages of the organic neuronic diseases. 

Two great forces underlie all of these primary organic degenera- 
tions. The one is the inherited and represents a diminished vitality, 
a lessened power of resistance against ordinary stimuli, or even extra- 
ordinary stimuli, in the constituents of the neurones; the other is the 
acquired and is revealed in the special virulence or vigor of the exciting 
cause. 

In most cases, both of these forces are in more or less operation 
at the same time, though in some affections, like Friedreich's disease 
for instance, the one will be the dominant factor, whereas in other 
affections, like locomotor ataxia, the other will be most in evidence. 

For the hereditary factor, with all its tendencies, Gowers has re- 
cently suggested the name abiotrophy and defined it as the "degener- 
ation or decay of parts in consequence of a defect of vital endurance." 
This defect of vital endurance characterizes practically all of the pri- 
mary organic degenerative diseases more or less. 

The process which seems to take place in the cell bodies is the 
same as, or is very closely related to, that which is technically called 
chromatolysis. This term is now employed to cover the alterations 
in the cell-body which we can observe and which are of the nature of a 
degeneration. They are not in any sense of the word inflammatory. 

Chromatolysis is a specific nervous phenomenon and is not wit- 
nessed in any other tissue of the body. There are various degrees 
of the process down to complete atrophy and annihilation of the cell. 
The accompanying illustrations show roughly, but forcibly the be- 
ginning of the chromatolytic process. The causes of these changes 
have already been dwelt upon in speaking of the degenerative process 
in general. Anything that profoundly disturbs the nutrition of the 
cell tends toward its chromatolytic modification. Hence an inheritance 
of poor vitality, a toxaemia of marked virulence, an exhaustive strain, 
or a tremendous shock may initiate it. 

A certain degree of chromatolysis usually occurs in cases of sec- 
ondary, or Wallerian, degeneration, as well as in those of primary 
degeneration. The proximal end of the neurone wastes somewhat while 



THE NEURONIC DISEASES 353 

the distal or severed end is disappearing. This is especially seen after 
amputations and in the rare conditions of neuromyelitis and ascend- 
ing degeneration of the motor nerves. This upsets in part the Wal- 
lerian law that when a nerve is severed from its nutritive center, the 
distal or severed end only undergoes degeneration : for here we ob- 
serve the proximal end also undergoing degeneration. As early as 
twenty-four hours after the damage is done to the peripheral nerve, 

FIGURE 54. 




A. 




A. Normal nerve-cell, stained by the Nissl method. (After Marinesco-Ray- 
mond. 

B. Disease of the cell after section of the peripheral nerves. Chromatolysis 
with nuclear displacement. (After Oppenheim.) 

changes have been observed, chromatolytic in character, in the related 
cell bodies of the medullary nuclei and anterior cornua. Restitution 
sometimes takes place; not infrequently complete atrophy occurs un- 
der these remarkable circumstances. 

The explanations offered for this phenomenon are all hypothetical 
though plausible. For example, it was for a time supposed to b 
sort of retrograde process, a backward-going Wallerian degeneration. 



354 THE NEURONIC DISEASES 

Many to-day believe, however, with Marinesco, Goldscheider, Len- 
hossek and others, that in health the nutrition of the cell is excited 
and maintained by the usual sensory and volitional impulses. When 
the cell is put out of action, as it were, by these peripheral degener- 
ative conditions, it is not called upon to functionate as it was wont to 
do, and is therefore not made the recipient of its wonted stimulus. Its 
nutrition therefore flags and it undergoes a chromatolytic deterioration. 

The observable phenomena in chromatolysis I have briefly de- 
scribed elsewhere. They consist first of a swelling and blurring of 
the cell, then of a shriveling up with a serration of its edges. The nu- 
cleus moves to one side (decentralization) and the nucleolus gradually 
disappears. The w r hole cell has its power to absorb staining reagents 
markedly lessened. The chromatin bodies move toward the periphery 
and the dumbbell-like bodies closely hug the edge of the nucleus. The 
latter bodies stain deeply. Vacuolation appears in the cell substance. 
As the process advances general atrophy of the neurone takes place 
and the latter finally disappears. If regeneration should occur, the 
reverse phenomena obtain, but much more slowly. The space that is 
left vacant is then filled with an overgrowth of neuroglia and connec- 
tive tissue (secondary sclerosis). In the secondary degenerations the 
cell-body undergoes a lesser degree or partial chromatolysis, though 
sometimes it may be complete and atrophic. The neuraxone, both that 
part of it "which has been severed from the cell and that which still re- 
mains attached, undergoes the well-known fibre degeneration; abso- 
lutely and completely in the former, relatively to the degree of the cel- 
lular chromatolysis in the latter. 

It is clear thus far that neuronic degeneration is a special patho- 
logical phenomenon and characterizes the nobler elements, the true 
nervous apparatus. The organic (observable) neuronic changes and 
the functional (non-observable) neuronic changes constitute the basis 
of the true nervous diseases, the diseases that belong to the nervous 
system per se. 

These diseases in all probability differ, so far as their being or- 
ganic or functional is concerned, in degree rather than in kind. There- 
fore, I have grouped these two great sets of diseases together and made 
a special class of them, calling them the neuronic diseases. 

We have just seen, however, that in the subclass of neuronic dis- 
eases, called the organic, the degenerative process is primary and sec- 
ondary in its origin. This of course is merely another way of saying 
that there are two great groups of causes that damage the nutritive 
function of the neurone and its several parts. The one group of 
causes go to the very fountain head of nutrition and overthrow it by 
directly hurting the cell-body. The other group of causes merely cut 
off, compress or otherwise mutilate the neurone and its processes so as 
to interfere with its vitality. Except in regard to heredity, we may 
say of both groups of causes that they are from without or are extra- 
neural. A toxin that sets up a primary degeneration is as much an ex 
ternal disease affecting the neurones secondarily as is a stab wound 
that severs the spinal cord and sets up a secondary degeneration. In 
both troubles the degenerations per se are the same, though their loca- 



THE NEURONIC DISEASES 355 

tions and immediate causes are different. A poison that initiates a 
primary polyneuritis, so-called, is really as much of an extraneural 
cause as is a cerebral embolus that cuts off the blood supply of a cer- 
tain area of cerebral neurones. The peripheral degeneration, as a 
mere disease process, is as much of a degeneration as that which oc- 
curs in the central trouble. 

It is obvious, therefore, that our classification of these degenera- 
tions into primary and secondary is quite artificial and is made only 
for coarse practical purposes. This is only too well demonstrated, and 
to our chagrin, when we try to decide whether a certain degenerative 
disease is a primary or a secondary one. We tacitly admit in such in- 
stances that the degeneration is one and the same but we can't make 
up our minds whether the causative factor is the primary or the sec- 
ondary one. How often this is the case ! It is perhaps best illustrated, 
however, in the development of our ideas in regard to locomotor ataxia. 
One hypothesis has declared that the degeneration of the peripheral 
sensory neurone is the direct result of the syphilitic virus in some way. 
Another hypothesis argues that it is due to a slow compression of the 
posterior nerve roots by the specifically inflamed meninges. The 
former explanation makes of tabes a primary degeneration ; the latter 
relegates it to a secondary degeneration from meningitis. 

Take as another illustration multiple neuritis. A degeneration of 
the peripheral neurones is observed in practically all cases. In the 
toxic cases it is sometimes a primary degeneration and due to a polio- 
myelitic process ; sometimes a secondary degeneration and due to a 
compressing interstitial inflammation. 

Landry's paralysis may be an initial stage of primary or secondary 
degeneration in the peripheral motor neurones. Ophthalmoplegia is 
both a primary and a secondary degenerative disease. 

The point I wish to emphasize by these and numerous other illus- 
trations that could be cited is that in these organic neuronic degenera- 
tions we have a sort of borderline group of diseases which lie between 
the purely inherent neuronic troubles, like the functional diseases, and 
the non-neuronic troubles like the inflammations and neoplasms that 
only affect the neurones secondarily and by compression. 

Therefore, it is difficult to classify positively all of the organic 
neuronic degenerations, for sometimes we behold them as primary pro- 
cesses, at other times as secondary processes. And yet I feel that the 
best interests of neurology will be subserved by a general classification 
founded, so far as present data will permit, upon the distinction be- 
tween the primary and the secondary organic neuronic degenerations. 

The two sets of diseases in which the primary and secondary 
neuronic degenerations respectively appear an- so dissimilar in respect 
to etiology, prognosis and treatment mat for this reason alone it seems 
to me most practical to emphasize the distinction by thus making it the 
basis of a classification. A degeneration of tin- pyramidal tracts from 
an intracranial hemorrhage may be no less serious, ; ,s a degeneration, 
than that which we see in amyotrophic lateral sclerosis, but the sec- 
ondary nature of the former and the primary nature of the latter in- 
sinuate an important distinction between them when it comes to the 



35^ THE NEURONIC DISEASES 

matter of their prevention by early treatment, or to the question of 
prognosis when they first begin to appear. Primary degenerations 
are usually hopeless, whereas secondary degenerations, especially if 
they don't implicate the nutritional function of the* neurone bodies, are 
comparatively hopeful. 

In taking up what I have termed the organic neuronic diseases in 
the next chapter, I have in mind especially the primary organic neu- 
ronic degenerations. The secondary degenerations will be incidentally 
referred to in the latter part of the book as the expected or accidental 
sequelae of the extra-neuronic diseases in which they happen to ap- 
pear. To illustrate, progressive muscular atrophy with its atrophic 
paralysis is regarded as a primary degeneration and is therefore classi- 
fied and treated here as an organic neuronic disease ; acute anterior 
poliomyelitis with a similar atrophic paralysis is regarded as an in- 
flammatory disease of the spinal cord and is therefore classified and 
treated elsewhere as a non-neuronic afTection. The neuronic degener- 
ation here is regarded as a secondary process, an early sequel as it 
were, of the infectious myelitis. 

Where a disease happens to be either a primary or a secondary 
degenerative trouble, it will be treated of most fully in the section 
wherein it would naturally fall by the greater prominence of the one 
or the other of its manifestations, and it will be only incidentally men- 
tioned in the other section. Moreover in this way, where the classi- 
fication O'f the disease is in doubt among the authorities, I will intimate 
my own opinion in regard to it. 

System Diseases. — The sharp localization of the lesion and its 
limitation to certain definite neurones is a remarkable characteristic of 
these organic degenerative diseases. The phenomenon has always 
aroused the greatest investigative enthusiasm among neurologists, and 
there have not been wanting plenty of hypotheses. To-day, however, 
we are as much in the dark as ever. Why such a general cause as 
heredity or toxaemia should provoke a degeneration in a particular set 
of neurones, and not in others, is still a profound mystery. And even 
in the secondary degenerations there is no adequate explanation as to 
why certain groups of neurones should be more implicated than oth- 
ers. If the explanation is to be found in a biological, evolutionary 
embryonic or developmental influence we are not yet in a position to 
adequately word our explanation. This is the same as saying that we 
do not know how heredity acts. I am convinced, however, that even 
in the inflammatory troubles with their so-called secondary 
degenerations, such as acute anterior poliomyelitis, though the 
location of the inflammation may be accounted for in some 
way by the peculiarity of the circulation in and through the 
anterior horns of the cord in this disease, the frequency with which 
certain of the cells, as those that preside over the tibialis anticus 
muscle, are affected, is due to some hidden biological fact, Mime spe- 
cial susceptibility conferred upon them by their evolution, their early 
use or their embryonic development. 

Certainly heredity plays a role, though perhaps a minor one. along 
with the infection, in these focal, inflammatory troubles with their 



THE NEURONIC DISEASES 357 

sharply localized secondary and permanent degenerations. In the 
purely hereditary troubles, like Friedreich's disease, we can go no 
farther than to say that an inherited biological or embryonal influence 
is at work. It would be perfectly useless to try and imagine why the 
brunt of the damage falls upon some neurones and not upon others. 
The fact is as much of an enigma as is the origin of sex. 

In regard to the organic degenerative diseases that follow a gen- 
eral intoxication, such as locomotor ataxia, we can make a guess, but 
only a feeble one, as to why the lesion is confined to a particular set 
of neurones. In this case we can reason behind the intoxication, as 
it were, and found our guess upon a biological and physiological basis. 
In some of them there is undoubtedly a localizing influence exerted 
by the heredity, along with the general strain or intoxication. 

If in the pure hereditary degenerative troubles certain groups 
of neurones are constantly broken down, it is but a fair conclusion to 
suppose that in some other acquired diseases, this same sort of heredi- 
tary influence may lie dormant, and does thus lie dormant, until it is 
rendered effective by the added presence of the depressing intoxica- 
tion. The question is often asked, for instance, why all, or even more, 
syphilitics do not develop locomotor ataxia, if syphilis be indeed the 
cause of this disease. One legitimate answer would be, though it 
would amount only to an inference drawn from analogy, that in cer- 
tain individuals who acquire the infection, there is an inherited weak- 
ness in the sensory system. The infection lowers the resisting power 
of the sensory neurones and immediately the hereditary tendency re- 
veals its presence and force. Another answer to the same question 
could be made in accordance with the Weigert-Edinger hypothesis. 
In this it is assumed that those neurones or systems of neurones, 
which are normally called upon to do more work than other systems, 
have the nice balance between their combustion and repair, their de- 
structive and constructive metabolism, more quickly and more pro- 
foundly upset than those which are not subject to such strenuous du- 
ties. Edinger argues that the sensory nervous apparatus is. compara- 
tively speaking, never idle and that certain parts of it are even more 
constantly in action than are other parts. For example, in locomotor 
ataxia the peripheral sensory neurones of the legs and eves are the 
chief points of the localization of the lesion because normally these 
neurones are incessantly in action in all of the performances of the 
waking state, reflex and voluntary. 

Of these two hypotheses, I prefer the former for several reas 
Edinger's theory does not answer the question why all syphilitics do 
not develop locomotor ataxia. It is to be presumed that the plrj 
logical strain upon their sensory apparatuses is approximately the same 
in all. Moreover the hypothesis omits entirely to account for the purely 
hereditary cases and those that begin to show their sharp localization 
even before the special neurones are actively called ii|x>n to work. 

If overwork is to he employed in explaining the localizatioi 
the lesion in these acquired troubles of adult-, the theory cannot 
tainly be laid aside entirely when the question involve ime sort 

of a lesion that appears early in life. I can much more readily un- 



358 



THE NEURONIC DISEASES 



derstand how heredity, strong or weak, may provoke the degenera- 
tions in Friedreich's disease and ordinary tabes, though it be the sole 
cause in the former and the partial cause in the latter, than can I con- 
ceive of a force determining a lesion in one disease such as super- 
function does, as it is claimed, in tabes, but doing nothing in another 
disease with a similar lesion such as the posterior degeneration ob- 
served in the Friedreich type of the trouble. Heredity can cover both 

FIGURE 55- 



ttndl 
Capsule 




"RooTs 

"Post 






Schematic representation of the neuronic structure of the motor and sensory 
pathways. (Modified from Jakob.) 

diseases in part at least ; but super-function can only be made to apply 
to one of them. If it be answered, however, that in Friedreich's dis- 
ease, the influence of excessive function is the proper explanation just 
as it is in locomotor ataxia, then we must assume that it accounts for 
the accompanying pyramidal degeneration in the motor tracts as well. 
If this is granted, then by analogy we ought to have the motor neu- 
rones more often degenerated in locomotor ataxia than we do. 



THE NEURONIC DISEASES 



359 



On account of these objections, I do not think, therefore, that the 
Weigert-Edinger hypothesis i9 as well supported as is the hereditary 
in explaining why certain groups of neurones are so much more liable 
to degenerate than others are when the same exciting causes are in 
operation. 

If the reader will recall the preceding chapter upon the neuronic 
architecture of the nervous system, and the illustrations that accom- 
pany it, he wall remember that the neurones were grouped together 
into various motor, sensory, commissural, associating and storage sys- 
tems. 

Lying side by side their cell-bodies formed the ganglia while 
their processes constituted the tracts. Each tract was made up of an 

FIGURE 56. 







Schematic representation of the neuronic structure of the sensory nerve tracts. 
(Modified from Jakob.) 

immense number of neuronic pathways along which the individual im- 
pulses traveled from one end to the other. In their course we learned 
that the impulses had to proceed step-like over two or more neurones, 
placed end-to-end, as it were, by synaptase, before they reached their 
journey's end. We analyzed two of the pathways about which we 
know the most, namely, the projection sensory and motor paths. We 
found that the former consisted of a number of neurones in apposi- 
tion, whereas the latter was made up of only two, the upper and the 
lower neurones. 

Our acquaintance with organic neuronic degenerations is entirely 
limited to the diseases of these projection sensory and motor path- 
ways. Doubtless there are similar degenerations in the commissural, 



360 



THE NEURONIC DISEASES 



association and intercalary systems of the brain and elsewhere that, 

for aught we know, underlie many obscure psychic and other troubles. 

We are far from being in a position to affirm that we know all 

of the degenerative diseases of the motor and sensory projection sys- 

FIGURE 57- 




leics 



/VWscl< 



terns. Even of those we do know we have still much to learn. Never- 
theless as the neuronic construction of these projection systems, so 
well shown in the accompanying diagrams, is such that the division of 
them into brain, spinal cord and nerve tracts is simply untenable from 
the clinical standpoint, we must, if possible, make the lines of divis- 



THE NEURONIC DISEASES 361 

ion correspond with the divisions between the individual neurones. 
On the motor side we can do this much more easily than we can on the 
sensory side, for the neurones that make up the individual pathways 
are much less in number and the points of separation between the two 
longitudinally related neurones are more uniformly and distinctly lo- 
calized. 

The upper neurones of the motor tract consist of a group whose 
cell-bodies lie embedded in the cerebral cortex around the fissure of 
Rolando and whose neuraxones pass down in a bundle through the 
internal capsule, the crura cerebri and the direct and indirect pyra- 
midal tracts of the cord. They all terminate in arborizations, but at 
various levels, in the column of gray matter that makes up the ante- 
rior horns of the cord and its homologous extension, the motor nuclei 
in the medulla oblongata. Their arborizations surround the cell- 
bodies found there. In this way, it will be observed that the cerebral 
cortex is brought into physiological communication with the cell- 
bodies of the lower motor neurones lying in the motor cranial nuclei 
and the anterior cornua. These variously lengthened upper neurones, 
taken all together, constitute what is called the Upper Motor Segment. 

The lower neurones of the motor tract are observed to have their 
cell-bodies where the neuraxones of the upper segment terminate in 
arborizations, namely, in the motor cranial nuclei and the anterior 
cornua of the cord. Their neuraxones pass out through the motor 
cranial nerves and the anterior roots and spinal nerves respectively. 
They terminate in the motorial end -plates of the various muscles to 
which they are supplied. In this way the entire somatic musculature 
of the body is brought into direct physiological connection with the an- 
terior horns of the cord and motor cranial nuclei, and into indirect 
physiological connection, through the upper motor neurones, with the 
cerebral cortex. These lower neurones, taken en masse, make up what 
is termed the Lower Motor Segment. 

The functions of these respective segments, though motor, are 
somewhat different, a fact which must be remembered when their dis- 
eases are clinically considered. The lower segment, through its indi- 
vidual neurones controls and stimulates the contractions of the indi- 
vidual muscles of the body. It also presides over their nutrition. \s 
its constituent neurones spring from various levels in the cord and 
from different motor cranial nuclei, the location of the lesion in a cen- 
tral disease can thus be determined by the particular muscle or the 
particular motor nerve that is symptomafically affected. 

Furthermore, disease of this lower motor segment, or of any of 
its constituent neurones, produces for obvious reasons a flaccid paraly- 
sis, a muscular atrophy and an electrical reaction of degeneration. 
Since these lower motor neurones serve as the efferent pathways t'<>r 
all the reflexes, their damage also causes a diminution or loss of all 
forms of reflex action. 

The principal organic degenerative diseases thai are limited to 
the lower motor segments, that we know of, and that will hi- discussed 
in the next chapter, are poliomyelitis, Wernicke's superior and inte- 
rior polioencephalitis, the acute ascending paralysis of Landry, asthenic 



362 



THE NEURONIC DISEASES 



bulbar paralysis or myasthenia gravis, and the primary degenerations 
of the cranial motor nerves, such as the ocular, facial, hypoglossal and 
motor branch of the trigeminal. 

FIGURE 58. 



N^uscle 



dcreie/l 




um 






The upper segment, through its constituent neurones, controls, 
stimulates and inhibits the activities of the lower segment. It does 
not influence, nor does it even know of, individual muscles. It pre- 



THE NEURONIC DISEASES 363 

sides only over systematized physiological movements. These move- 
ments are produced by the combined action of a number of physiolog- 
ically related muscles. 

The distinction between the functions of the upper and lower seg- 
ments in regard to these physiological movements and the individual 
muscular contractions is of immense importance in clinical practice. 
I am in the habit of teaching that the upper motor neurones are 
psychic, so to speak, in their activities and, like the mind, are cogni- 
zant of general movements only, such as those of the leg or of the 
hand, whereas the lower motor neurones are wholly spinal and are 
cognizant only of individual muscles, such as the deltoid or the quad- 
riceps femoris. 

The upper motor neurones do not enter into the production of an 
ordinary reflex, though by reason of their inhibitory control over the 
lower neurones they inhibit the normal reflex somewhat. They do 
not exert any special trophic influence, though it is assumed that their 
normal stimulant action upon the lower neurones helps in a measure 
to preserve the latter 's proper nutrition. 

Remembering then the relationship, anatomical and functional, of 
the upper motor segment to the lower, we are not surprised to discover 
that when it is diseased and its inhibitory control is thus withdrawn 
from the lower segment, the muscles are thrown into state of spastic 
rigidity or spastic paralysis; that this paralysis implicates muscle 
groups which subserve the movements of various parts of the body like 
the face, the arm, the leg or the whole half of the body, but does not 
Implicate merely individualized muscles ; that the reflexes are exag- 
gerated ; that there is little or no muscular atrophy; and finally that 
the normal electrical reactions remain unchanged. 

The more important organic diseases of the upper segment thai 
we know of and that will be treated of here are the spastic paralyses of 
adults and of children, hereditary spastic paraplegia, Erb's spinal 
paralysis, some secondary spastic paralyses and briefly hysterical spas- 
tic paraplegia. If Strumpell's cortical polioencephalitis be listed, 
though there is some doubt as to its existence, it will have to be in- 
cluded here among the secondary degenerations. 

There are a number of diseases that involve the entire motor tract. 
both upper and lower segments. Foi obvious reasons the dominant 
symptoms will be those of the lower motor segment. To this, how- 
ever, there is one exception, namely, the type of progressive mil- 
iar atrophy which Charcot named amyotrophic lateral sclerosis. Here 
the disease process seems to begin in the lower end of the upper motor 
segment and hence for a time the dominant symptoms are those of an 
upper motor segment disease. 

The troubles that we usually classify as involving the whole mo- 
tor tract are the progressive muscular atrophies, progressive bulbar 
paralysis, the progressive muscular dystrophies and the amyotrophic 
lateral sclerosis. 

The sensory tract is far more complicated than the motor and in 
regard to its organic degenerative diseases we are not well informed. 
We are best acquainted with those that belong to the peripheral neu- 



304 



THE NEURONIC DISEASES 



rones of the system, namely, locomotor ataxia, tic douloureux, some 
neuralgias about which, however, there is considerable doubt, and the 
primary degenerations of the nerves of special sense, especially the 
optic. 

FIGURE 59- 













The best way to indicate the construction of the various pathways 
that make up the sensory system will be to trace an impulse along 
them from the skin to the brain. The accompanying diagrams will 
assist the reader in following the courses of the impulses. 



THE NEURONIC DISEASES 365 

Leaving the skin and passing first along the sensory nerve, a stim- 
ulus arrives at the posterior spinal ganglion where the cell-body of 
the respective neurone is found. Up to this point the impulse has 
been traveling' by way of a long, modified dendrite. After it leaves 
the cell-body in the posterior ganglion it emerges along the neuraxone 
•of the same neurone that passes directly into the cord by way of the 
posterior root to arborize around a group of cells embedded in the pos- 
terior horn. From this second cell, and by way of its neuraxone, the 
impulse, crosses through the anterior commissure to the lateral column 
of the opposite side where it ascends in the antero-lateral ascending 
tract of Gowers to finally pass through the medulla and pons and 
to arborize around the ceil-bodies nesting in the optic thalamus. Con- 
tinuing on through this third cell and its neuraxone, it ultimately 
reaches the cerebral sensory cortex. 

This is what is called a direct sensory path and it consists of the 
three end-to-end neurones, the peripheral, the spino-thalamic and the 
thalamocortical. 

Another direct pathway is that up the columns of Burdach and 
Goll to the nuclei, cuneatus and gracilis, at their summits, thence to 
the thalamus, and so on to the cortex. The peripheral neurones in these 
instances are of enormous length and actually extend from the skin, 
through the posterior root, to the top of the posterior columns of the 
cord. 

There are certain sensory impulses from the muscles, the joints 
and the viscera that reach the brain through a very much more in- 
direct route than the two just outlined. The^e indirect pathways are 
not well known and we can only trace the impulses along them in a 
tentative sort of a way. Entering the cord by way of the posterior 
roots, the latter ascend the posterior columns to their respective nuclei, 
thence they cross to the opposite side in the sensory decussation, some 
ultimately reaching the cerebellar cortex where they terminate, others 
continuing on from the cerebellar cortex to the red nucleus, optic thal- 
amus and cerebral cortex. Other impulses of this sort ascend to the 
cells of the column of Clarke, thence to the cerebellum by way of the 
direct cerebellar tracts, and so on to the brain. These indirect paths 
may be summarized thus, peripheral sensory neurone, spinocerebellar 
neurone, cerebello-thalamic neurone, and thaJamo-cortica] neurone. 

Along the direct paths are supposed t<> pass all the sensations "i" 
touch, temperature and pain; along the indirect travel the impulses 
from the muscles, tendons and joints that have to do with coordina- 
tion and the maintenance of equilibrium and tin- activities of the vis- 
cera. 

My excuse for introducing here this minute account Off tin- sen- 
sory pathways is that they are all implicated apparent!) in the - 
sory system disease about which we know the most, namely, locomo- 
tor ataxia. Further details in regard to tin- anatomy and physiology 
of these various projection pathways will Ik- found in the chapters de- 
voted to the physiology of the brain and spinal cord. The considera 
tion of the neuronic structure of tin- special sense systems will not be 



3^6 



THE NEURONIC DISEASES 



taken up in detail here as it belongs to the description of the various- 
cranial nerves later on. 

There are quite a number of organic neuronic degenerations that 

FIGURE 60. 







Stniory Nerve 
jtom NVusclf etc. 



crxsory 
Nerve' 

j^onTViScerx 



occur in a combined way in both the sensory and motor systems. Chief 
among these are amaurotic family idiocy, some forms of hereditary 
cerebellar ataxia, Friedreich's disease, ataxic paraplegia, the primary 



THE NEURONIC DISEASES 367 

combined sclerosis of Putnam, toxic combined sclerosis, progressive 
interstitial hypertrophic neuritis of children, multiple neuritis and 
neuromyelitis. 

Some authors are perhaps justified in classifying among these or- 
ganic neuronic degenerative troubles, because of the frequent 
prominence of their systemic manifestations, syringomyelia, 
infantile diplegia from agenesis, delirium grave or Bell's 
mania, and dementia paralytica. I prefer for the present not to do so, 
however, because it seems to me that the extra-neuronic manifestations 
are sufficiently prominent to still keep them entirely out of this class. 
Their neuronic changes, except perhaps in a few exceptional cases 
of Bell's mania are, in my judgment, emphatically secondary. 

DISEASES OF THE AFFERENT OR SENSORY SYSTEM. 
LOCOMOTOR ATAXIA. 

Locomotor ataxia is a better name for this disease than either 
tabes dorsalis or posterior spinal sclerosis. All three are objectionable 
however. It is not a motor trouble, as might be inferred from the first 
name. It is not a wasting of the back, as the second suggests. And 
it is not primarily a posterior spinal sclerosis. As the ataxia, shown in 
the gait, is the most obtrusive symptom, the name locomotor ataxia 
is perhaps the most convenient to employ. 

The disease consists of a slow, progressive degeneration in the 
peripheral sensory neurones, and their related structures, with a secon- 
dary sclerosis of the sustentacular tissues. Clinically it is character- 
ized by certain sensory phenomena, incoordination of movement, and 
trophic disturbances. It is notable for the absence of all true motor 
symptoms and mental aberrations. 

Etiology. — Since the initial work of Fournier, Erb and others, 
the opinion has been growing that syphilis is the cause of locomotor 
ataxia. Tersely stated, the hypothesis would be, — no syphilis, no loco- 
motor ataxia; or in other words, every case of locomotor ataxia pre- 
supposes syphilitic infection. Many do not accept entirely this dictum 
because no sets of statistics have yet been brought forward in which a 
positive history of syphilis was obtained in every case. Even Four- 
nier and Erb admit this, but as such a history is obtainable in at least 
75 to 85 per cent, of all cases, they and others assume that it has 1>een 
overlooked in the remaining 15 or 25 per cent. This is not improbable 
as syphilis is sometimes innocently acquired and honestly denied. At 
other times it reveals such slight and evanescent primal*} and 
ondary manifestations as to be very easily overlooked. It is not abso- 
lutely true, however, as is frequently asserted, that it is in this class of 
syphilitics that locomotor ataxia is most prone to occur. While a con- 
servative opinion would not agree with Fournier that locomotor ataxia 
is parasyphilis or metasyphilis, a mere sequel of constitutional syph- 
ilitic infection; and much less with Lesser, who believes that it rep- 
resents a fourth stage of syphilis, thereby being in no sense a separate 
and distinct entity of itself, it does accept the Statement that syphilis 
is far and beyond all others a cause of locomotor ataxia. 



368 THE NEURONIC DISEASES 

Some of the conservatives hold that the specific infection serves 
simply as a predisposing cause and in that sense may underlie most 
of the cases. Other causes, however, must come into play along with 
the specific to provoke the disease under discussion. 

A still larger number of conservatives argue that in the 15 or 25 
per cent, of cases in which a history of syphilis is not obtainable, the 
other causes may and probably do produce tabes without the existence 
of an underlying specific, predisposing factor, such as syphilis. 

That syphilis precedes the appearance of tabes in a large majority 
of cases is undeniable. That it is an antecedent demonstrable in all 
cases, has not yet been shown. Therefore, that it is the only cause of 
locomotor ataxia is still an open question. 

The other causes that are believed to act in conjunction with 
syphilis and in occasional cases possibly alone, are excesses of all 
kinds, especially excessive venery, occupations, such as that of the syph- 
ilitic driver whose ataxia began in the right arm, exposure to prolonged 
cold and dampness, strains of all kinds, such as running a machine, 
climbing arduous steeps, difficult parturition with hemorrhage, pro- 
longed lactation, depressing emotions, and spinal injuries. Simple 
traumatic tabes is to be regarded with doubt. 

Apart from syphilis, other infections have been credited with the 
disease, namely, pneumonia, rheumatism, typhus fever. Most tabetics 
have had gonorrhoea but it is not a cause. Latent syphilis may have 
been present in all of these cases for where such causes are discov- 
ered apart from syphilis they, like ergot when used in excess, produce 
an atypical form of the disease or a combined type of degenerative 
sclerosis. 

Heredity does not play a significant part in the etiology though 
it is believed by many that an inherited neuropathic predisposition goes 
far toward explaining why some syphilitics acquire locomotor ataxia 
and others do not. 

Men are^more frequently attacked by the disease than women, in 
the proportion almost of ten to one. This may be because of the greater 
liability of men to the various causes spoken of above; and yet the 
difference is so marked that a special susceptibility is believed by many 
to belong to the male. 

The disease appears preeminently in the middle period of adult 
life. More than half of the cases occur between the ages of thirty and 
fifty. About thirty-seven seems to be a favorite year for its commence- 
ment. It has been observed as early as ten or twelve years of age, 
and as late as sixty-five. It is exceedingly rare, however, before twenty 
and after sixty. 

In some mysterious, probably biological, way, race and nationality 
appear to exert an influence upon its development. In the Negro, the 
Jap, the Egyptian, the Bosnian and the Herzegovinian, the Kirgizh 
and the natives generally of East and Southeast Africa, among whom 
syphilis is rife, tabes is all but unknown. This has been used as an 
argument against the syphilitic etiology of the disease ; but it may be 
counter-argued that it is because syphilis in these races has effected an 



THE NEURONIC DISEASES 369 

immunity on account of its very excessiveness and almost universality, 
against its own tertiary accidents. 

Pathology and Pathogenesis. — If syphilis is the cause, medi- 
ately or immediately, of locomotor ataxia., the lesions found are not 
those commonly recognized as syphilitic. Hence, tabes is not a syph- 
ilitic affection in the strict anatomico-pathological sense. The degener- 
ation that is known now as the primary process of the disease is a 
remote result of the specific intoxication, the wreckage, as it were, 
after the storm. Most of the syphilitic cases reveal their first symptom 
in from five to fifteen years after the acquisition of the infection. In 
a large number of these cases the signs of syphilis have been slight 
and when the tabetic manifestations had begun to appear were prac- 
tically nil. Only the suspicion of an initial lesion can be formed some- 
times. In women usually this is wanting. Erb, Fournier and others 
have noticed that in a few case? in which no history of syphilis could 
be secured, the father was syphilitic. 

The term tertiary as applied to the disease in the sense of be- 
ing a late manifestation of syphilis, is misleading, for the primary 
infection may precede the outbreak of the trouble anywhere from one 
to forty years. 

The most prominent and constant post mortem finding in loco- 
motor ataxia is the degenerated appearance of the posterior spinal 
columns. Burdach's columns, especially in the lumbar and dorso- 
lumbar regions, and Goll's columns higher up. are seen to be graver, 
smaller, harder and less punctated than normally. A narrow ventral 
area just alongside the posterior commissure escapes the change. 
Clarke's vesicular columns, Lissauer's tracts, and the posterior corn u a 
are included in old cases of the disease. This can all be readily ob- 
served with the naked eye. This pathological picture is what misled 
the earlier investigators into giving the names to the disease that they 
did and in placing it among the spinal cord affections. 

Two things are to be distinctly noted in regard to the pathological 
basis of locomotor ataxia, as we know the disease to-day. They are, 
first, that the disease is not an inflammation, but a pro^ressiz'e defen- 
eration, and secondly, that this degeneration occurs in the peripheral 
sensory neurone, whose cell-body rests in the posterior root ganglion 
and whose processes extend out into the peripheral nerve on the one 
hand and up into the posterior tracts of the cord on the other. The 
degeneration may be looked for anywhere in the entire cutaneo-spinal 
extension of this neurone. It is more often found, however, in the 
outer or cutaneous end and the inner or spinal end than anywhere in 
the middle or in the cell-body. It is most frequently observed in the 
spinal end. As these spinal end- extend up int.) the posterior columns, 
it is clear why in the great majorit) s, these columns are the 

principal seat of the disease. 

Microscopically this symmetrical, bilateral posterior degeneration 
is seen to originate in the nerve fibre- and run through the usual c >urse. 
The neuroglia may remain normal but as a rule it proliferates along 
with the connective tissue. A few remaining fibre> may be seen run 
ning through the proliferated tissue. The bloodvessels <!«. nol exhibit 



370 



THE NEURONIC DISEASES 

FIGURE 61. 




^-i.a '- 



Locomotor ataxia. Cervical section.. Dorsal section. Lumbar section. (After 
Jakob. 



THE NEURONIC DISEASES 371 

any signs of congestion, vascular irritation or inflammatory change. 
The degeneration of the nerve elements, with the secondary sclerosis. 
can be traced into Clarke's column in some cases, into Gowers', antero- 
lateral tract in others, and even into the direct cerebellar tract in a 
still smaller number. The posterior roots are often degenerated and 
the posterior ganglia also in a few cases. The anterior roots are not 
affected or only so in very late and complicated cases. In the latter 
the degeneration is seen in the pyramidal tracts and other anterior and 
lateral areas of the cord also. The peripheral nerves, especially those 



FIGURE 62. 



'.A.* 




Atrophy of the posterior root and of the spinal ganglion in tabes dorsalis. 
h. H', posterior root. ( Weigert's stain.) (After Oppenheim.) 



of the leg, in advanced cases exhibit signs of degeneration, degenera- 
tive atrophy or neuritis. Whether this cutaneous degeneration is pri- 
mary or secondary is not yet established. When the disease pn 
has reached into the medulla, the degeneration may be I in 

;he spinal roots of the fifth cranial nerve, and often in the solitary 
bundle and posterior vagus nucleus. Rarely the auditory and h; 
glossal nuclei may be wasted. The nuclei of the third nerve have been 
implicated. Among the cranial nerves, however, the optic is n 
often the one affected. The Gasserian ganglion, the nerves of the 
ocular muscles, the vagus, the recurrent laryngeal and the hyp 
have all been broken down in some case-. The membrar j the 

posterior surface of the cord and around the 
chronicallv inflamed. 



$J2 THE NEURONIC DISEASES 

In regard to the modus operandi of the syphilitic virus in pro- 
ducing these lesions and in lighting up the degenerative process that 
constitutes the basis of the disease we know nothing positively. Va- 
rious hypotheses have been offered from time to time but none of them 
satisfactorily explain all of the. conditions present. Most of them have 
been entirely abandoned. Two, however, are still regarded with some 
favor, and to a certain extent are yet on trial. 

Marie long ago put forth the view that the syphilitic virus affects 
the nutritive function of the peripheral sensory neurones by directly 




Sagittal section through the spinal ganglion with the posterior and anterior 
roots and efferent nerves. (Weigert's stain.) (After Oppenheim.) 



poisoning, or otherwise damaging, their cell-bodies found massed to- 
gether in the posterior spinal ganglia. This being the case the ends 
of the neurones farthest removed from the nutritive centers, namely, 
the cutaneous ends on the one hand and the spinal ends on the other, 
naturally waste and degenerate first. The objections to this hypothe- 
sis are that the degenerative process here represents something more 
than what would be the result of a mere malnutrition of the neurone 
produced by a disturbance, of the nutritive function of its cell-body : 
that it is not supported by sufficiently constant or uniform changes 
within the posterior spinal ganglia ; and that it fails to explain the 
greater frequency of the degenerative process in the spinal end of the 
neurone and its relative infrequency in the cutaneous end. Though 



THE NEURONIC DISEASES ^>7 3 

Marie has himself lately given up this hypothesis it still seems to be 
somewhat in favor in some quarters. 

Redlich and Obersteiner, noting the constancy and the character 
of the degeneration in the posterior roots and the frequency of the 
adjoining meningitis, propounded the theory that a chronic specific 
meningitis of the posterior parts of the cord is the primary disease. 
This meningitis, by constricting, compressing and otherwise injuring 
the roots where they pass through it sets up an atrophy in them and 
thus transmits the disease by contiguity up into the cord. This hypothe- 
sis brings locomotor ataxia into line with the established forms 
of spinal syphilis by making of it primarily a vascular disease, a spe- 
cific meningitis. Many of the earlier symptoms, especially the pains, 
are not unlike those observed in meningitis involving constriction of 
the posterior roots. The objections to the theory, however, are that 
it fails to explain the almost universal limitation of the meningitis 
and its associated degenerative sequelae to the posterior parts of the 
cord (though Marie and Guillain have latelv invoked the peculiar vas- 
cular and lymphatic supply here to solve this difficulty) ; that it ac- 
counts for a degenerative process that ought accordingly to appear 
more frequently in other forms of chronic specific and non-specific men- 
ingitis ; and that it fails utterly to explain the not infrequent associated 
degeneration of some of the cranial nerves, as for example the optic, 
and the peripheral cutaneous nerves, and of the posterior spinal ganglia. 

Every explanation hitherto advanced leaves without an answer 
the question as to why the disease, whether it be syphilitic or not in 
origin, begins and limits itself to the sensory neurones, and 
especially to the lower sensory neurones. Biology, embry- 
ology, evolution and heredity have all been invoked to show 
that there is a special, neuropathic weakness in these particular neu- 
rones and that therefore they yield to the virus of the syphilis. The 
Edinger theory endeavors to cover the ground. In it the assumption, 
first noted by Weigert, is made that certain parts of the nervous appa- 
ratus are worked more than others with consequently a more rapid 
disintegration and consumption of the •elemental metabolism. This 
occurs in the sensory system which is ceaselessly transmitting im- 
pulses from the periphery to the brain. Under the stress therefore of 
such a universal depressing agent as syphilis, the sensory system is 
the first to give way. 

Symptoms. — Xo case of locomotor ataxia presents exactly the 
same clinical picture as any other case. The variations in the combi- 
nation of symptoms and their character are innumerable. Tims arbi- 
trary types of the disease have been described, much to the confusion 
of its diagnosis. There is, however, a fairly definite symptomatology 
and keeping well in mind this typical picture, oik- can easily recognize 
the slighter shades of variation which i' may under 

I will first attempt a description of the typical presentation of 
the disease and then discus- a little more in detail a few of its varia- 
tions. It must be remembered that the symptoms in all cases will be 
those that one would naturally expect from a slow, progressive 



374 THE NEURONIC DISEASES 

generation here and there in a widely extended, peripheral sensory 
apparatus. 

Progressive sensory disturbances form the basis of the sympto- 
matology of tabes. These may begin and remain in the legs ; they may 
extend to the arms; or they may commence in and be limited to the 
arms. They may involve the sensory nerves of the head and of the 
viscera. Later symptoms may diverge from the purely sensory type so 
that trophic, motor and vasomotor manifestations may be present. The 
uniformity of the symptomatology of tabes depends upon its sen- 
sory character and upon its steady progressive course; its variability 
depends upon the variations in the location of the degenerative pro- 
cess. While the former tempts us at times to make a diagnosis upon 
the barest indications, the latter should warn us not to do so unless 
two or more symptoms are present. A mere pain, a mere diplopia, a 
mere loss of knee-jerk or a mere loss of vision, without any other symp- 
tom to base a diagnosis upon, even when there is a history of syphilis, 
ought never to more than arouse a suspicion of possible tabes. Only 
in this way can mistakes be minimized in the diagnosis of a disease 
which assumes such a variety of outward forms. 

The first indications of locomotor ataxia usually make their appear- 
ance in from five to fifteen years after the contraction of the syphilis. 
Ten years is about the average. The patient notices a feeling of weak- 
ness and tiredness in his legs, especially after a slight exertion, not un- 
like that seen in neurasthenia. He observes that in writing or button- 
ing his clothes he has not quite his usual control over the fingers. 
Along with these suspicious manifestations there may appear here and 
there about the body slight fugitive momentary pains that are mistaken 
for cold and rheumatism. On the other hand, none o<f these symptoms 
may be present, but the patient begins to worry about his slowly failing 
eyesight, with the occasional attacks of temporary diplopia. One or 
both eyelids may droop slightly. In other cases even before the above 
warnings have arisen, there may have been noticed for awhile excessive 
sexual desire, satyriasis, followed by rather rapid and alarming im- 
potence. The bladder often manifests a slight disturbance. The urine 
comes slowly. The weakness, the fugitive pains, the bladder irregular- 
ity, the sexual impotence or the failing eyesight usually sends the pa- 
tient to a physician, who makes a careful examination and finds other 
very suggestive and objective signs of an incipient tabes. 

A convenient classification of the symptoms may be made upon 
the progressive character of the disease. We speak of a pre-ataxic, an 
ataxic and a paralytic stage. These are not by any means sharply 
defined from one another. They overlap and the symptoms of one may 
be found in another. Furthermore, there is nothing definite as to the 
duration of any one of the stages. They are only uniform in respect 
to the successive relationship that they bear to each other. 

The pre-ataxic stage of locomotor ataxia is the all-important stage, 
both in the interests of the patient and to the credit of the practitioner. 
In the ataxic stage the disease has already progressed so far that a 
diagnosis is comparatively of slight value to the patient and of little 



THE NEURONIC DISEASES 375 

honor to the diagnostician. In the paralytic stage it is of no special 
moment to anybody. 

Therefore the earliest manifestations of the disease are of the great- 
est importance and must be sought for and studied with the keenest 
acumen. 

The symptoms, named in the order of their frequency, which par- 
ticularly characterize the pre-ataxic stage are loss of the patella-reflex 
(Westphal's sign), lancinating pains. Argyll-Robertson pupil, anes- 
thesia and analgesia and static ataxia (Romberg's sign). 

Other symptoms that may appear in this stage, though they are not 
so constant as those named, are bladder disturbances, sexual weakness, 
diplopia from ocular paralysis, gastric and laryngeal crises, paralysis of 
the vocal cords with spasmodic cough, optic atrophy and even trophic 
changes in the joints and bones. 

My own observation confirms that of most writers of large experi- 
ence that the loss of the knee-jerks is a relatively constant and early 
symptom. It is found in about 05 per cent, of the cases. It is not 
always the first symptom by any means, though it is the most frequent 
among the initial symptoms. Diminution and loss of the knee-jerk 
occurs in many other diseases, as, for instance, neurasthenia, peripheral 
neuritis, anterior poliomyelitis, complete transverse myelitis in the d 1 
lumbar region. I saw it absent once in an unusually healthy young 
woman, though Oppenheim doubts whether it is ever a normal phe- 
nomenon. In locomotor ataxia the loss is usually complete from the 
beginning and cannot be modified by any known means of reinforce- 
ment The ankle reflex occasionally precedes the patella reflex in van- 
ishing. When both are gone the loss of the ankle-jerk may be more 
absolute than that of the knee-jerk. Both phenomena continue through- 
out the entire course of the disease. They may be observed tor a time 
in rare instances upon one side only. 

Very many authorities declare that the lancinating pains are the 
first and the most frequent symptom of locomotor ataxia ( Bramwell, 
Goldflam and others). The statistics of Mott. Starr. Robinson and 
myself show that they occur in only about 60 or 80 per cent, of the 
cases. As Oppenheim well points out, the intrinsic value ^i this symp- 
tom is lessened somewhat because of its subjective character. Neverthe- 
less, when the pains are present their character and distribution can 
hardly be mistaken. They are quick, sharp and distre* I he) arc- 

characterized as lancinating, lightning-like, fulgurating. They are mo 
mentary in duration, appear in most unexpected spots and dn no! follow 
the anatomical distribution of any particular nerve- or set of nerves. 
They may be frequent and succeed one another with great rapidity in 
the course of a number of hours or days. Then the\ may remain awaj 
for many hours, days, weeks or even months, onl) to reappear again 
in all their pristine severity and freakishness. They have to hi- endure 1 
in any part of the body, though in the vast majorit) of the cases the) 
occur in the legs. The trunk suffers next in frequency with them, then 
the arms, and lastly the thighs, [ntense hyperesthesia is sometii 
located where the pains have occurred. 

As the disease advances the pains gradually lessen and become 



376 THE NEURONIC DISEASES 

of a dull, boring character. Late in the ataxic stage, and all during 
the paralytic stage, they are practically absent. When they attack the 
viscera, the sexual apparatus, the anus, most peculiar descriptions may 
be given of them. They have been known to be present as long as 
twenty-five years before the onset of any other manifestation of the 
disease. The victims sometimes become habituated to them and go 
regularly about their business in spite of them. They are in such cases 
often imagined to indicate rheumatism, neuralgia and other painful 
affections. This fact and their entirely subjective character suggest 
most vehemently that as a single diagnostic sign they can awaken 
nothing more "than a strong suspicion of locomotor ataxia, though, on 
the other hand, they must never be assumed too positively as the pains 
of any other disease. 

The Argyll-Robertson pupil, or the pupil that is irresponsive to 
light but readily responsive to convergence and accommodation, is, in 
importance as a symptom of locomotor ataxia, second only to West- 
phal's sign, though it is not so constant as the latter. It is ofttimes a 
very early symptom and may even precede all the others by a long 
period of time. The phenomenon may be observed in only one eye or 
it may be more marked in one eye than in the other. Occasionally it 
is preceded by a sluggish or weakly responsive pupil. It occurs in 
about 80 per cent, of all cases. Sometimes it is present when there is a 
loss of the cutaneous reflex contraction of the pupil. Myosis and, less 
frequently, mydriasis may accompany reflex iridoplegia. According to 
Rochon-Duvigneaud and Heitz, myosis is regularly accompanied by a 
simple Argyll-Robertson, that is to say, the contraction to convergence 
is perfect ; but mydriasis is always accompanied by a complicated 
Argyll symptom, or one in which the contraction to convergence is ab- 
sent or defective. In both the reaction to light, of course, is totally 
abolished. Though this remarkable form! of reflex iridoplegia is some- 
times witnessed in general paresis and in acquired or congenital syphilis, 
it is so much more common in tabes that with any other single symptom 
it may be adopted as the ground for a positive diagnosis. It may be the 
only important sign of those present. 

Oppenheim regards analgesia, with or without impaired sensibility, 
as one of the four cardinal symptoms of the first stage. There is no 
question that disturbances of the pain sense, tactile, temperature and 
muscular senses may all appear early and prominently. In the order 
of their frequency these sensory phenomena appear about 
as follows: Various parcesthesicc and numbness, girdle-sensation, 
anesthesia and analgesia, loss of muscular sense. Various combina- 
tions, however, are exhibited by different patients of anaesthesia, anal- 
gesia, hypaesthesia, hypalgesia, hyperaesthesia, hyperalgesia and re- 
tardation of the sense of touch, pain and temperature. 

When the cases come actually under examination it is probably true, 
as stated by most authors, that tactile anccsthesia is the most frequent 
and constant sensory disturbance. In the extremities it is usually of the 
blunted, stocking or gauntlet type. In the trunk it consists of bands 
or partial bands of anaesthesia to touch only, and not pain, also, as is the 
case sometimes in the limbs. Hitzig first called attention to this symp- 



THE NEURONIC DISEASES 377 

torn, but we are indebted to Laehr, Patrick and others for its special 
investigation. The anaesthetic area does not correspond with the 
cutaneous distribution of intercostal nerves, but with the innervation as 
represented by the spinal cord segments. It is more horizontal than 
is the course of the spinal nerves. These bands are of varying width 
and run from the median line toward the axillary line. When numer- 
ous they suggest, considered together, a sort of broad girdle disturb- 
ance. 

This trunk anaesthesia may conservatively be said to occur in about 
80 per cent, of all cases. According to Mott trunk atussthesia is present 
in all cases with gastric crises and covers mostly the zones of four or 
five dorsal roots. As the upper cervical roots of the brachial plexus 
are rarely diseased, it seldom extends above the second intercostal 
space. 

Thermo-ancesthesia is far less frequently met with than tactile an- 
aesthesia and analgesia. 

The Romberg symptom or static ataxia, swaying with the eyes 
closed, belongs to the latter part of the pre-ataxic stage. It occurs in 
about 80 per cent, of cases. It is well brought out, and its pathological 
origin well emphasized, by the simple manoeuvre, suggested by Oppen- 
heim, of having the patient, with his eyes shut, bend his back and then 
straighten himself again. 

The other symptoms that are occasionally observed in the first 
stage of the disease, with or without one or more of the above, may 
appear for the first time in any stage and so will be discussed after I 
have finished the picture of the disease in its entire course. 

The first stage or any particular symptom of the first stage may 
last many years before the onset of the ataxic stage. There are often 
periods of quiescence in the course of the* disease or new pre-ataxic 
manifestations make their appearance. As the trouble progres 
however, the pains become more sharp and frequent, the sexual im- 
potence becomes complete^ the gait develops a slight uncertainty, vis- 
ceral and laryngeal crises become alarming, vision gets duller, deep 
numbness replaces the paresthesia? and possibly slight changes begin 
to be noticed in the joints. The symptoms that were already present 
become, as a rule, more pronounced. The disease shows decidedly that 
it is progressing. 

When the symptoms have reached the stage at which tin- incoor- 
dination of movement is distinctly noticeable, the patient i» said to 
have arrived at the second or ataxic period. In this period all of the 
earlier manifestations that were presenl become more marked, except 
the pains and crises, which now diminish both in severit) and 
quency. The ataxia is the great symptom of this stage and - far over 
shadows all the others that Duchenne was led by it to give the name to 
the disease that he did. It should n«>t he forgotten, however, th;it 
though the incoordination is the mOSl <>l>vi"iiv symptom, it i> n.t by any 
means the most important. 

Ataxia appears in the legs in about J$ per cent, of all cases, and 

in the arms in aboul 8 per cent. The symptom occur in othei affections 

than tabes, notably in multiple neuritis, disseminated cerebrospinal 



37% 



THE NEURONIC DISEASES 



FIGURE 64. 



FIGURE 65 




Trunk anaesthesia in locomotor ataxia. 



THE NEURONIC DISEASES 379 

sclerosis and cerebellar disease. When it has appeared, however, in 
the course of tabes, the disease is usually so far advanced that there are 
other indications present which render the diagnosis a comparatively 
•easy one. The affection at this time has reached its full development. 
The movements of the arm or leg will be observed to be full and strong. 
In other words, there is absolutely no motor paralysis. In walking the 
patient exhibits a decided uncertainty, especially if the room be dark- 
ened. In fact, it is sometimes quite impossible for him to get about at 
all in the night. Occasionally the trouble is first noticed by the patient 
when he ascends or descends a flight of steps. He stumbles unaccount- 
ably. Not rarely it is noticeable objectively before the patient himself 
is aware of it. A momentary closing of the eyes, or a looking away 
from the floor or neighboring wall increases the ataxia so much that it 
is all but impossible to walk. In walking the patient lifts his leg 
"higher than it is necessary, rotates it slightly outward, jerks it forward, 
stamps it down upon the floor with the heel first and the toes last. 
When he is seated the ataxia is observed as soon as he is asked to kick 
the leg of the table. 

With the hand he finds it difficult to perform the more delicate and 
•complicated movements, such as writing, buttoning his clothes or touch- 
ing the end of his nose quickly when his eyes are shut. 

Ataxia may involve the facial and tongue muscles, though only 
very rarely. 

More significant still are the spontaneous movements, which are 
sometimes seen in the ataxic arms or legs. They are entirely involun- 
tary. The patient cannot keep his limbs quiet. The arm suddenly rises 
to an elevated position or the hand is lifted up, and all without the pa- 
tient's knowledge if he happen not to be looking. According to Hirsch- 
berg, these weird movements are not the result of a complication, but 
are a manifestation of the incoordination. Like the latter, they are 
increased when the eyes are closed. 

The duration of the ataxic stage may be many years and, like the 
preceding period, be characterized by intervals of apparent quiescence 
or slight remission in the progress of the disease. 

As the second period draws towards its close the incoordination 
becomes so bad that it is quite impossible for the patient to move about 
at all. In a short time he takes to his bed and the disease passes into 
the so-called paralytic stage, which, as a rule, is much shorter than 
either of the other two. The pains have at last ceased. The eyesight 
is almost entirely gone. The anaesthesia and the analgesia are extensive 
and profound. The bladder and the rectal function., are most seriousl) 
disarranged. Trophic disturbances result in obstinate ulcers, bed-sores, 
muscular wasting and especially softening and disease of the bones and 
joints. Distortions and spontaneous fractures are seen in this stage 
The muscular scum- is lost and the stereognostic mux- is gravely dis- 
turbed. Anosmia and deafness even may be present. With all this, 
however, there is still no actual paralysis if the case is an uncomplicated 
one. The mind unfortunately remains clear as a rule, though in some 
cases it happily becomes clouded or weakened. The patient grows 
abnormallv emotional Thus be lridden, foolish, wasted, a physical and 



3 8o 



THE NEURONIC DISEASES 

FIGURE 66. 







I 




Locomotor ataxia. From a photograph in the Pathological Museum of the 
Med. Department of the University of Illinois. 



THE NEURONIC DISEASES 38 1 

mental wreck, the victim lingers helplessly on a few months more until 
■complete exhaustion from bedsores, cystitis, pyonephrosis or some other 
intercurrent malady mercifully puts an end to the sad picture. 

There are symptoms that may appear at any time in the course of 
a locomotor ataxia and be indicative of the disease : but they are not 
as constant nor as frequent as those just referred to. Though they are 
of less value in the establishment of the diagnosis, they are strongly con- 
firmatory when they constitute a part of the composite picture. Oc- 
casionally they may appear alone or early in the disease. They may be 
unaccompanied for a long period of time by any other symptom. Under 
such circumstances they should always awaken a suspicion of tabes 
and keep the attendant on the alert to detect the slightest manifestation 
of any other sign that will confirm the suspicion. 

Bladder disturbances ma}' be among the earliest symptoms. They 
occur in about 60 per cent, of the cases. Among my own cases this 
was a very frequent symptom. At first there is a little difficulty in 
micturition. The patient cannot void his urine when he feels he ought 
to. Then again he may feel a desire to void it too frequently. Grad- 
ually the trouble increases until in the later stages of the disease actual 
incontinence and retention occur. In some cases this trouble disap- 
pears in spite of the progressive character of the malady. An early 
bladder disturbance coming on several years after syphilitic infection 
should always be mistrusted. 

Constipation usually, and for the same reason, accompanies the 
vesical trouble. 

The early satyriasis and impotence I have already referred to. 
Oppenheim has seen an involuntary priapism continue for weeks at a 
time. Nocturnal attacks are not uncommon. Impotence usually follows 
all such manifestations and is generally complete inside of a year. I 
am convinced, however, that too much stress is placed by the pro- 
fession upon the sexual disturbances as a sign of tabes. I saw a case 
of advanced locomotor ataxia with all the typical symptoms, early 
pains, Westphal sign, Argyll -Robertson pupil and extreme ataxia pres- 
ent, which several physicians declined to pronounce tabes because there 
was not, and never had been, the slightest disturbance of the sexual 
function. In women a sort of nymphomania sometimes occurs par- 
oxysmally and is spoken of as a clitoric crisis. 

The so-called crises are important phenomena. They occur in the 
earlier periods of the disease. As their name in part indicates, they are 
sudden, unexpected, temporary disturbances of a more «>r less violent 
nature and sensory in origin, in the viscera and visceral function-. In 
the order of their frequency they may be listed about as follows: ( ias- 
tric, rectal, laryngeal, pharyngeal, intestinal, cardiac, renal and bladder. 

The gastric and laryngeal crises are the more important, the former 
on account of their frequency (36 per cent, in Mott's cases), and the 
latter on account of their alarming character. All of the other crises 
are comparatively rare. In the gastric crises the patient experieno 
sudden, twisting, wrenching pain in the region of the stomach. He 
nits first his food, then gall. He grows pale and weak, and shows 
by the rapidity of his pulse and generally that he is in great distress. 



382 



THE NEURONIC DISEASES 



The crisis passes after several hours, or it may be days or weeks, as 
suddenly as it came on. There is no foretelling when it may reappear. 
Trunk anaesthesia can be discovered in all cases with gastric crises. 
Usually these, as well as the other crises, alternate with the lancinating 
pains and sometimes are accompanied by a slight fever. 

The laryngeal crisis occurs much less often. When seized by it the 
patient chokes and coughs suddenly and for a few minutes experiences 
a paroxysm, with cyanosis, such as occurs in pertussis. The attack is 
sometimes very severe and distressing and the victim feels as if he were 
about to die from asphyxia. The laryngoscope discovers nothing ab- 
normal. Paralysis of the laryngeal muscles, especially of the crico- 
arytenoidei postici, has been observed late in tabes. 

A rectal crisis occurred in 8 per cent, of Mott's cases. It consists 
of sudden pain and evacuation, or of colic with diarrhoea. 

Abrupt disturbances of deglutition are regarded as pharyngeal 
crises. 

The implication of the vago-accessorius nerve is shown by the oc- 
casional cardiac and respiratory crises. There is a sharp, quick pain 
near the heart, with a sudden feeling of oppression and a rapid, irregu- 
lar pulse. Angina pectoris is not unfrequently suspected, so similar are 
the two phenomena. 

Pain in the chest, with disturbances of the respiratory function,, 
may occur. In a case observed by Egger in Dejerine's clinic a brachyp- 
nrea had lasted at least four years. The respirations were reduced to 
seven or eight per minute for two or three hours after eating. Vomit- 
ing, roughness of the voice and tachycardia were also* present. 

Renal and bladder crises are characterized by sudden, sharp pains 
in the region of those organs. Pel and Oppler have described respec- 
tively a temperature crisis. 

Optic nerve atrophy probably occurs more frequently than some 
collections of cases of tabes state. It is a symptom that is not objective- 
ly noticeable and is not often enough sought for. Mott found it in 
30 per cent, of the cases of hospital tabes examined by him. Among" 
Starr's cases it was found in about 9 per cent. The average, calculated 
from the statistics of numerous observers, is about 20 per cent. It is 
sometimes a very early symptom and has been known to precede all 
other signs for many years. It may occur in any period of the disease. 
It is a serious trouble, as it is often the forerunner of brain involve- 
ment. The absolute reliability of Benedikt's dictum, that tabetic symp- 
toms usually recede or come to a standstill when optic atrophy makes 
its appearance, is open to grave doubt, though in some instances it does 
seem to be true. The beginning atrophic changes can sometimes 
be detected with the ophthalmoscope when the vision is but little inter- 
fered with. The atrophy is of the simple, progressive type and in 
uncomplicated tabes is never preceded by optic neuritis. There is no 
swelling or hyperemia of the disc. It generally is first visible in the 
temporal halves and gradually involves the whole field. At first the 
ncuteness of vision is good and there are no central scotomata for colors 
or white. The visual field is gradually, concentrically and sector-like 
narrowed. Sooner or later complete blindness comes on ; in the ma- 



THE NEURONIC DISEASES 383 

jority of cases in about three years. One eye may be affected sooner 
than the other, but as a rule the degeneration is bilateral. 

Ocular palsies are the most frequent cranial nerve symptoms of 
tabes. Any ocular muscle, or muscles, may be involved, so that the 
paralysis is never £n associative one~ In the earlier period of the dis- 
ease it is apt to be transient ; later on it becomes chronic and permanent. 
Diplopia, ptosis, strabismus and even nystagmus are met with. Oph- 
thalmoplegia may occur, as well as myosis and mydriasis. 

The trophic phenomena that occur in the course of locomotor ataxia 
are important. They are late symptoms usually, though they have been 
seen in the pre-ataxic stage. Of these the arthropathies, Charcot joints, 
are the most significant and occur in about 10 per cent, of the cases. 
The knee-joint is probably the most frequently affected. The phenom- 
ena may, however, be seen in the hip-joint, the shoulder, the elbow, the 
ribs, the ankle and the spinal column. In many respects the trouble 
resembles an arthritis except that the latter is accompanied by pain, 
redness and fever. In the Charcot joint a sudden swelling comes on, 
with a profuse accumulation of fluid; the intra-capsular tissues are 
destroyed ; the capsule loses its power of contraction ; and a condition 
resembling a luxation or subluxation supervenes. New substance is 
found in the joint, and either as an excrescence or free causes a more or 
less marked deformity. Under these circumstances the long bones are 
brittle so that spontaneous fractures are frequent. 

The perforating ulcer, most commonly located in the ball of the foot 
and often bilaterally in both feet, is a trophic tabetic symptom. Other 
rare manifestations of this character are spontaneous gangrene, spon- 
taneous falling of the nails, nutritional disturbance of the skin, falling 
out of the teeth, ulceration of the mucous membrane of the mouth 
with alteration of the sense of taste, neuroparalytic keratitis and other 
trigeminal manifestations, herpes, facial hemiatrophy and forms of 
muscular atrophy. These are all comparatively rare symptoms. Some 
of them, as, for instance, the muscular atrophy, may be extensive and 
involve the whole body. Multiple neuritis (Dejerine) is probably the 
cause of them, though many hold that they are true spinal cord symp- 
toms. 

Unilateral hyperidrosis, ecchymosis or suggillation and various 
exanthems have been reported, though it is questionable whether they 
are true tabetic symptoms. 

Cerebral symptoms occur in the course of tabes, but they arc indica- 
tive of a complication. They should be noted, nevertheless, because 
they often modify the true tabetic symptoms. The anaesthesia and anal- 
gesia are naturally different when there are psychic aberrations pi 
cnt, from what they would be otherwise. Sudden attacks d\ ven 
congestive, apoplectiform, epileptiform and migrainous seizures, acute 
mania with slight changes of character, hallucinations, even visual 
hallucinations with complete optic atrophy, ma\ all occur in tain 
They indicate, however, a cerebral complication. Mich as cerebral 
syphilis or incipient dementia paralytica. 

Diagnosis. — The diagnosis of locomotor ataxia is n<»t difficult in 
typical and in advanced cases. Only in the early period of the disease 



3^4 



THE NEURONIC DISEASES 



is confusion encountered. One ought never to doom a patient to so 
hopeless a malady unless two o<r more signs are positively present. 
Not even an Argyll-Robertson pupil or a loss of the patella reflex alone 
will warrant a diagnosis. A simple, progressive optic atrophy is prob- 
ablv the strongest single indication of a probable* tabes, but even it 
should only awaken a strong suspicion. Two or more symptoms, 
therefore, must be observed before a positive diagnosis can be offered. 
The combinations that these symptoms may assume, the groupings 
which they may exhibit, are almost innumerable. Care, thoroughness 
and a recollection of the cardinal, sensory-trophic character of the dis- 
ease, if exercised in the examination of every case, will result in a 
minimum amount of error in diagnosis. 

A careful comparison of the symptomatology of locomotor ataxia 
with that of neurasthenia, hysteria, hypochondriasis, aberrant forms of 
exophthalmic goitre, chronic myelitis, spinal tumor and hereditary 
ataxia will enable one to make easily a differential diagnosis between 
these affections. The Westphal sign, the Argyll-Robertson pupil, the 
lancinating pains, the analgesia, the optic atrophy, the transient diplopia, 
the crises and the ataxia are all characteristic. 

Among the affections that do give rise to considerable trouble may 
be mentioned especially multiple neuritis, syphilitic pseudo-tabes or 
spinal syphilis, multiple sclerosis and general paresis. Moreover, these 
diseases may be associated with the tabes, a fact which sometimes adds 
immensely to the difficulty of the diagnosis. 

In multiple neuritis there is a history usually of an intoxication 
(alcohol, lead, arsenic), or an infection (tuberculosis, fevers), rather 
than of syphilis. There is a true, flaccid paralysis. There are local 
pains, elicited by pressure upon the nerves and muscles. The muscles 
exhibit a high degree of atrophy early and the electrical responses are 
characteristically altered. In many cases of multiple neuritis a peculiar 
psychosis occurs in which amnesia, disorientation, confabulation and 
pseudo- reminiscence are notable. 

Perhaps the greatest difficulty is met with in distinguishing a 
syphilitic pseudo-tabes, or spinal syphilis, with simulation of tabes, from 
true tabes. Syphilis and parasyphilis are not identical in the usual 
acceptation of the terms. One is not even a complication of the other, 
though they both may be present in the same patient. Nevertheless, 
whether so associated or not, they sometimes have many symptoms in 
common and lead to a confused diagnosis. It is probable that most 
of the reported cures or improvements in locomotor ataxia that have 
been credited to heroic doses of mercury and iodides were made possi- 
ble because the cases were really cases of syphilitic pseudo-tabes and not 
of true tabes. Collins has ably pointed out that syphilitic pseudo-tabes 
may be diagnosed when one or another symptom is of disproportionate 
severity; when the tendon-jerks behave peculiarly, as, for example. 
being absent on one side, exaggerated on the other or returning after 
a period of absence ; when symptoms of implication of the lateral por- 
tion of the cord are superimposed upon those of tabes, especially when 
such symptoms are associated with unilateral mydriasis or unilateral 
reflex iridoplegia ; whenever there is considerable or permanent im- 



THE NEURONIC DISEASES 385 

provement under antisyphilitic medication ; and finally whenever there 
is an association of motor paralysis (save transient ocular palsy) with 
the symptoms of tabes, whether it be dependent upon brain, medullary 
or cord lesion. 

1 once saw a case of multiple sclerosis diagnosed as locomotor 
ataxia by able diagnosticians. When the lesions involve the lumbar 
cord especially, the ataxia, the loss of patella reflex, the pains may all 
be looked for. Under such circumstances search well for intra-cranial 
symptoms and note the characteristic involvement of the upper extremi- 
ties. Sooner or later nystagmus, dysarthria, tremor, paretic rather than 
sensory incoordination, intentional choreiform jerking and increase of 
tendon reflexes in the upper extremities will enable one to recognize 
the case as disseminated sclerosis. 

As is well known, general paresis is closely related, pathologically 
and symptomatically, to tabes. In many cases of the spinal disease 
the onset of mental symptoms indicates the complicating presence of 
the cerebral affection. Sometimes both sets of symptoms make their 
appearance together in the beginning. The diagnosis has to wait often, 
under such circumstances, before it can be positively determined which 
disease is to predominate. In spite of the presence of optic atrophy, loss 
of knee-jerks and the Argyll-Robertson pupil, the existence of mental 
manifestations, speech disturbances, fibrillary tremor of the tongue arid 
apoplectiform attacks points to dementia paralytica. As I have said 
under the symptomatology, pure tabes may in some cases be accom- 
panied by mental manifestations. These, of course, are not to be con- 
founded with paresis. 

Prognosis. — Locomotor ataxia being a slow, progressive, degen- 
erative disease, it is prolonged in its course and its prognosis, while 
favorable as to life, is exceedingly bad as to recovery. There seem 
to be periods of quiescence during the course of the malady and usuall) 
the greatest hope that dare be entertained, either with or without 
treatment, is to bring on such a temporary cessation of the general 
advance. A large number of cases terminate in about tin years. Some 
have lasted twenty-five years or more. Death is generally the result 
of exhaustion, cystitis, pyelonephritis, decubitus, infection or other in- 
tercurrent trouble, as in most of these chronic degenerative maladies. 

In the first stage of the disease recovery as a very rare event may 
occur. The earlier the stage and the less severe the symptoms tin- 
better the chances. In this stage many of the cases, with proper care, 
may become stationary and endurable for a long time. 

In the second stage the prognosis is hopeless SO far as any change 
for the better is concerned. Still this stage is not always unbearable. 
The patient can sometimes get about and even attend to business. I »' 
the disease continues quiescent during this stage or during the greater 
part of it, the patient may carry on the activities of a fairly useful 
citizen and not be entirely unhappy. Such a state of affairs ma\ last 
for years. 

In the third stage there is absolutel) no more hope, hut rather ai, 
outlook for an early termination. 

It has been noticed that a certain prognostic value ma\ he place 1 



386 



THE NEURONIC DISEASES 



upon particular symptoms. For instance, an early optic atrophy usu- 
ally means a long duration of the disease; a quick development of 
bladder trouble and ataxia indicates a much shorter course, and possi- 
bly an early death ; severe lancinating pains and gastric crises produce 
an exhausting and wearing strain upon the patient's general nervous 
system and so hasten the end. 

The disappearance of the pains, of the ophthalmoplegia, of the 
crises and of other symptoms, notwithstanding the onward course of 
the disease, must not deceive the physician in regard to the prognosis. 

Treatment. — The treatment of locomotor ataxia is limited. In 
the early stages, before the ataxia has appeared, an attempt at a cure 
may be made ; especially if the tabetic symptoms have shown themselves 
within two years of the primary specific infection, are not very severe 
or rapidly progressive, and are associated with other manifestations 
indicative of active syphilis inside or outside of the nervous system. 
A few complete cures have been reported under such circumstances, 
though it is a question whether the diagnosis was correct or whether 
the cure, so-called, was not in the syphilitic manifestations rather than 
in the tabetic. In the large majority of instances treated thus early 
the most favorable result obtained was the cessation of the course of 
the malady. In a disease that is so steadily progressive and whose 
primary lesion is a neuronic degeneration, even such a result as a 
temporary cessation of the onward advance is to be looked upon as a 
happy event, notwithstanding the fact that such a result is knowm to 
occur now and then without treatment and thus divides the credit with 
the treatment. 

It is in the first stage that the most troublesome of all questions in 
the therapy of locomotor ataxia presents itself — namely, whether or 
not to use antisyphilitic medication. I am satisfied that if the symp- 
toms are entirely tabetic and they have appeared two years after the 
infection, the administration of mercury and the iodides will do no 
good, but may do a great deal of harm. If the lancinating pains are 
unusually severe and frequent, and especially if the onset of the ataxia 
is abrupt and early, the above remedies are absolutely contraindicated. 
When in doubt it is safer in tabes to withhold all antisyphilitic medica- 
tion than to experiment with it. Even if it be granted that tabes is 
nothing but a fourth stage of syphilis, as some extremists are begin- 
ning to teach, and not mere parasyphilis as Fournier used to maintain, 
it is a form of syphilis that seems to be beyond the reach of mercury and 
the iodides. 

All of these suggestions are doubly applicable to the ataxic stage of 
the disease. In the paralytic stage they are not even up for considera- 
tion. 

After the first stage the treatment is entirely general and symp- 
tomatic. Even in the first stage symptomatic measures have a high 
degree of applicability. 

No treatment of locomotor ataxia is to be commended in which 
rest is not an important factor. It is often a very perplexing question 
as to how much rest is to be enjoined. In the earlier stages of the dis- 
ease I believe the more the patient keeps quiet the better it will be for 



THE NEURONIC DISEASES 387 

him. In the ataxic stage it is not always so imperatively necessary. 
In the third stage it is forced upon him by his paralytic condition. 

When recommending rest we must be careful not to alarm un- 
necessarily by making it too absolute. In fact, a certain amount of 
exercise, short of the awakening of the feeling of weariness, a con- 
tinuation as far as possible in the business and social affairs of life, 
an avoidance of the thought that he is doomed to a life-long invalidism, 
are best for his mental and physical welfare. He should be urged to 
lead a life of great moderation, regularity and even tenor. All forms 
of stimulation, excess and dissipation must be absolutely forbidden. 
Sexual excitement must be prohibited and an early, ataxic had better be 
urged not to marry. I saw a case of advanced tabes in a married man 
who continued to hold intercourse with his wife without any apparent 
ill effects. Shortly after her death he consulted me in regard to the 
possible effect upon his ataxia of the continuation of his sexual activity 
illicitly. Of course, there could be but one answer to such a question. 
Cases of this sort are exceptional. 

Alcoholic stimulants and even tobacco had better be given up in the 
interests of health. 

A man's occupation must receive some consideration. It should 
be changed if it is confining, exhausting or dangerous. I urged a 
bricklayer with only a partial Argyll-Robertson reaction, loss of knee- 
jerks and an occasional lancinating pain, to give up his trade at once 
for obvious reasons. A clerk who was obliged to sit all day in a 
cramped position was persuaded to seek some mild form of occupation 
that took him more into the open air. 

Monotony, whether mental or physical, must be avoided. With 
the avoidance of a mental or physical form of monotonous activity, 
brief intervals of absolute rest, lying prone upon a couch, should be 
arranged for, especially during the pre-ataxic stage and when the pain- 
are frequent and lively. 

The bodily nourishment must be maintained at the highest pitch 
by the use of plain, nourishing food, with but a modicum of tea and 
coffee. 

Refreshing sleep, long and often, should be encouraged in every 
possible way. 

Amusements, entertainments and games, rural pleasures and sum- 
mer resort delights must all be indulged in with great moderation and 
always without provoking too marked emotional excitement. Moun- 
tain climbing and sea bathing are risky and had better not be in- 
dulged in. 

Hot and cold baths should not be taken, but the regular use of 
tepid bathing to keep the skin clean and active is to be favored. 

The functions are all to be looked after and kept as near health} 
rctivky as possible. 

In a word, quiet, moderation, abundance of fresh air and g<«>d food, 
and all the forces that go toward the creation and preservation of con- 
stitutional vigor, with alternations of moderate exercise, with plent) 
of rest and sleep, are the chief elements in the general treatment 
tabes. Rut this is not all, for the symptomatic treatment is always an 



388 THE NEURONIC DISEASES 

important factor and often the only part of the therapy that the physi- 
cian is called upon to exercise his special knowledge in. 

The drug treatment of tabes is extremely unsatisfactory. Many 
remedies have been proposed and tried, but none of them has retained 
the universal approval of the profession. Most of them were sug- 
gested long ago when our knowledge of the pathology of the disease 
was scanty. It was thought that somehow they would overcome or pre- 
vent the sclerosis which was believed to be the primary trouble. Now 
that we know the fundamental process is a slow, progressive, paren- 
chymatous degeneration, we are not surprised at the successive disap- 
pointments caused by one vaunted remedy after another. Of all these 
general alteratives the nitrate of silver. has remained in favor the long- 
est. It may be given by the mouth or hypodermically. It must be 
given for a long period of time, with frequent intervals of rest to 
prevent argyria. The dose is about a quarter of a grain in pill. Ergot, 
potassium iodide, the double chloride of gold and sodium, phosphorus, 
belladonna, arsenic and barium have been used. I have not seen any 
benefit that could be clearly attributed to any one of these numerous 
preparations. The nitrate of silver is the only one of the group that 
I would deem worthy of a trial. Some of them, such as arsenic, small 
doses of phosphorus, the tincture of iron, may be given for their gen- 
eral tonic effect. Erb counsels strongly against strychnine, and most 
justly so in regard to the use of it in large or even average dosage. 
On the other hand, I believe that strychnine in very minute doses, not 
over one two-hundredth of a grain three times a day, when added to 
rest and other general measures, is a most valuable remedy. In larger 
doses it may be absolutely disastrous. It must always be employed with 
caution and one had better err on the side of giving too small than too 
"large doses. 

The use of the extracts of gray matter, especially the gray matter 
of the sheep's brain, as long ago recommended by Constantin Paul, to 
regenerate atrophied nerves, moved Leyden to recall humorously the 
similar experiments with products furnished by the ass in Pliny's time. 
The same atmosphere of the comic surrounds the use of Brown- 
Sequard's testicular fluid, the goat lymph and the other startling agents 
now more or less in vogue. These primary, degenerative neuronic dis- 
eases, progressive and hopeless, offer a glorious field for the unscrupu- 
lous catch-penny and the ignorant quack. 

The largest opportunity for the drug treatment of locomotor ataxia 
is in the management of its special symptoms. The lancinating pains 
are the symptoms that the patient most vehemently demands relief from. 
They are sometimes excruciating, they are always wearing and ex- 
hausting. Ofttimes if they are mitigated but in part he can learn to 
bear them and for years may go about his ordinary avocations in spite 
of them. The remedies that have from time to time been recommended 
for their relief are now almost legion. Most of them will give rise to 
disappointment. Sometimes one will succeed in one case, only to fail 
in another; hence it is well to have a full armamentarium ever at 
hand. The opiates and morphine are to be avoided as long as possible, 
for fear of establishing a dangerous habit; and yet they arc the most 



THE NKI KON'IC DISEASES 389 

effective agents we have to combat the pains with. At times they 
must be used, but always cautiously and for as brief a period as possi- 
ble. After the opiates the following remedies may be mentioned : 
Codeine, sodium salicylate, cantonin, chloride of aluminum, acetanilid. 
antipyrin, phenacetin, methylene blue, analgen, salipyrin, lactophenin, 
pyramidon, exalgine, phosphorus, solanin, cannabis indica, neurcdin and 
bicarbonate of sodium. Here as elsewhere the axiom holds true that the 
multiplicity of remedies is in inverse proportion to the benefit obtained 
from them. Most of the above drugs will prove disappointing in the 
majority of cases. Exceptionally this or that one may be found effica- 
cious. 

The crises usually need special attention. The local application of 
cocaine for the laryngeal crises, and the hypodermic injection of mor- 
phine for the gastric, are the readiest means of affording relief. So 
unsatisfactory are all other measures that one is disinclined even to try 
them, and yet morphine must be withheld from a tabetic patient as 
long as his endurance holds out. 

Bladder and rectal pains may be combated with suppositories of 
iodoform and belladonna, codeine, antipyrin, ichthyol, warm injec- 
tions, etc. 

Morphine and oxalate of cerium may be used for the attacks of 
vomiting. Nothing will prevent their coming on. 

For insomnia the usual remedies, such as the bromides, chloral, 
paraldehyde, hyoscyamus, are all commendable. 

In a word, the symptomatic management of tabes is no different 
from the symptomatic management of any other disease. It is only 
somewhat more resistant and therefore calls for more powerful reme- 
dies, such as morphine, which very remedies must be avoided. ( hie 
must not employ his strongest agents too early in the battle, but reserve 
them until later when the struggle grows fiercer and all other measures 
have completely failed. 

Hydrotherapy is highly commendable in all cases of tabes, if em- 
ployed intelligently and with a certain degree of regularity. The 
chief benefits from the water-cures of this country and of Europe are 
due to the systematic method of application usually carried out, and not 
to any special medicinal virtues in the water. Sometimes it is positively 
dangerous for a patient to go to one of these establishments, for, being 
absent from his regular attendant and under the care of those who are 
responsible for a large and varied assortment of patients, he is apt to be 
neglected or to urge forms of heroic treatment that may hasten the 
onward progress of his malady. The good that these establishments 
afford can just as well he obtained at home if the patient is tractable. 
For ten or fifteen minutes every day a tepid bath is both grateful and 
health-giving. Brine and carbonized baths are excellent. I lot baths 
must never be taken. Sweat and vapor baths, recommended by Leyden 
for early tabes, had better be employed with great caution. Not baths 
are one of the dangers of the springs and resorts that have been rei 
mended. As a rule the temperature of the water should never be al 
95 degree^ I\ (old baths and cold douches are approved of by some 
authorities. Krb treated nineteen patients with cold baths, of whom 



390 



THE NEURONIC DISEASES 



sixteen were benefited. It is a question, however, whether the risk run 
does not outweigh the benefit obtained. Erb affirms that a bath with 
a temperature above 58.5 degrees F. is positively injurious. Cold wet 
cloths to the lower limbs, their immersion in cold water after a pre- 
liminary warming with warm, moist wrappings, are less objectionable 
than a cold full bath. The water may be from 48 to 66 degrees F. 
The time of the immersion should be not longer than a minute. The 
limbs should be vigorously dry-rubbed and kept at rest afterwards. 
Stimulation of the cutaneous circulation is the object aimed at in this 
manoeuvre. Cold spinal douches I would never recommend. They may 
prove harmful. 

Electricity has been happily used in some cases of locomotor ataxia. 
Care and moderation must be observed here also. All forms of elec- 
tricity and all modes of application have been tried. Central galvaniza- 
tion of the spine and general faradization is a combined method that 
exercises both a tonic and beneficial reflex effect upon the nervous 
structures. Three or four times a week, eight or ten milliamperes of 
the galvanic current may be transmitted through the spine with one 
pole at the neck, the other at the lumbar region. No sitting should 
be prolonged beyond five minutes and the treatment should be kept lip 
for many months. Static electricity and the faradic brush are some- 
times acceptable to the patient. Pains and anaesthesia have been re- 
lieved in this way. The current should be strong enough to provoke 
slight pain, but not muscular contraction. As a symptomatic remedy 
electricity has a wide field of usefulness ; as a curative measure it is 
about as valueless as all other remedies. There is danger in its use, as 
with all other measures, if it is applied too frequently and too heroically. 
The indication for massage in tabes is as a general tonic. Massage 
of the skin improves its nutrition and may partly relieve some of the 
sensory manifestations. Deep massage of the muscles is useless and 
debilitating to the patient. It is to be employed only when paralysis and 
atrophy begin to show themselves late in the disease. Passive motion 
is contra-indicated where the articulations are already too mobile, and 
the muscles are in a hypotonic state. There is not much of a field for 
massage in tabes and when it is tried it should be very gentle, and the 
seances very short. Exhaustion is a condition to be studiously guarded 
against in tabetics and massage is most dangerously liable to provoke 
exhaustion. 

The suspension treatment introduced a few years ago by Motschut- 
kowsky and popularized by Charcot has not fulfilled the promises it 
first held out. Temporary effects, such as relief of the pains and im- 
provement in the gait, follow its application in some, indeed in very 
many, instances. But they all relapse. The modus operandi of the 
effect of the treatment upon the degenerating nerve elements is any- 
thing but clear and in some respects the treatment is unscientific and 
irrational. However, it is still used to some extent under a modified 
form, such as drawing the legs forcibly up over the patient while he is 
lying on his back (Benedict), or approximating the patient's chin to his 
flexed knees (Blondel), or with the lees extended and adducted. bend- 



THE NEURONIC DISEASES 391 

ing the upper part of the patient's body forcibly forward while he is 
seated on the edge of a table (Gilles de la Tourette). 

Operative nerve stretching, once popular, has been completely dis- 
carded as a therapeutic measure. The wearing of a corset has relieved 
the pains in some instances, and according to Bramwell tabetics with 
much ataxia sometimes walk better in India rubber soled shoes. 

Of all the mechanical measures used Fran J? el's re-education exer- 
cises are the most in vogue to-day and indeed do seem to afford the best 
results. They relieve, however, only the ataxia. Their psychic effect 
on the patient is good and they improve the muscular strength. They 
are useful in all stages of the disease. The exercises are simple in 
principle, though in details they may be greatly elaborated. Blocks of 
wood placed on the floor, short flights of steps, ladders for the practice 
of the legs, keyboards, simple buttoning and unbuttoning of the clothes, 
picking up of specially distributed articles for the exercise of the arms, 
are some of the simple forms of apparatus that may be extemporaneous- 
ly arranged. A little ingenuity will suggest means by which the patient 
for a few minutes every day can practice the function of coordination in 
his legs and arms. This, like all other methods of treatment employed 
in locomotor ataxia, must not be expected to accomplish too much. In 
some cases it seems to be without any effect. It should always, how- 
ever, be given a faithful trial in all cases. 

Even hypnotic treatment has been suggested in this disease. Beril- 
lon, of Paris, proposed it in 1895 because of certain functional psychical 
factors. The proposal is not such an absurd one in view of the fac 
that many believe the benefit that temporarily accrues from the use of 
suspension, gymnastics, Frankehs exercises and other measures is 
largely psychical. The restoration of confidence, the awakening of 
hope and the anticipation of improvement are all beneficial in this dis- 
ease and doubtless are in part the explanation for some of the g 
derived from treatment, whether the treatment be given by the scientific 
physician or the quack. This, taken in conjunction with the well- 
recognized characteristic of this disease to cease progressing at times, 
leads to the erroneous reports of cures. 

Unfavorable as the prognosis is in this disease, it is the duty of 
the medical man to use all his best efforts to keep its victims out of tin 
hands of frauds and religio-medical charlatans. He can do >" b) en- 
couraging the patient, keeping up hi> anticipation and strengthening 
his confidence in every way. The quack does this \^\- his <>wn persona] 
gain; the physician should do it as a part of his general management 
of the trouble because he will thus keep the patient in the hands of 
those best able to care for him — namely, the medical profession, he 
cause the nature of the disease is such as to warrant a certain amount 
of hopefulness, and finally because such a state of mind exercis< 
certain degree of positive benefit in minimizing the symptoms and in 
retarding their progress. 

OTHER SENSORY DEGENERATIVE DISEASES. 

We do not know of any other primary systemic sensory degenera- 
tive troubles. It is not improbable, however, that they ma) 



39 2 THE NEURONIC DISEASES 

There are some forms' of psychosis and certain epileptiform manifesta- 
tions with pure sensory phenomena, like hemicrania sometimes, that 
suggest a possible intracranial sensory systemic trouble. A degenera- 
tive affection is rarely limited to the sensory cranial nerves. x\s a rule 
such degenerations constitute a part of tabes, dementia paralytica, mul- 
tiple sclerosis, syphilis and other general diseases, or they are a sec- 
ondary result of inflammatory and other extra-neuron ic processes. 
Primary disease, however, has been observed, though very rarely, in 
some of the cranial nerves. The optic and the trigeminal nerves have 
probably illustrated the condition most frequently. Perhaps some few 
instances of tic douloureux could be classified here. The neuralgias,, 
however, as I have shown elsewhere, are something more than mere 
nerve troubles of a purely local character, and this is preeminently true 
of tic douloureux. Primary, bilateral optic atrophy does occasionally 
occur, though it is much rarer than secondary or associated atrophy. 
The auditory nerve has been supposed to have been primarily affected,, 
but if so it must have been very exceptional. Primary disease in the 
glosso-pharyngeal, pneumogastric and sensory spinal nerves is prac- 
tically unknown. In general toxic and infectious states they are oc- 
casionally degenerated, especially the vagus. With secondary degenera- 
tion they are not infrequently affected. 

DISEASES OF THE EFFERENT OR MOTOR SYSTEM. 

a. DISEASES OF THE WHOLE MOTOR TRACT. 

PROGRESSIVE MUSCULAR ATROPHY. 

There are a number of affections in which wasting of the muscles,, 
with a resulting paralysis, is the dominant and often the sole feature. 
Unlike the association of the paralysis and atrophy observed in acute 
poliomyelitis and neuritis, in the diseases now about to be considered 
the combination is one of atrophy and paralysis. In other words, the 
wasting in the former follows the paralysis, in these the paralysis 
follows the wasting and proceeds pari passu with it. Many of the for- 
mer diseases, in fact most of them, are purely inflammatory in character 
and the neuronic degeneration is a mere secondary result or sequel. 
In these, however, the degeneration appears to be a pure primary 
process throughout. 

It will be remembered that the efferent or motor path extending 
from the cerebral cortex to the musculature of the body consists of 
two anatomically separated grand divisions. 

The upper segment is made up of a group of neurones whose cell- 
bodies nest in the cerebral cortex, while their axones, of various lengths, 
extend downward through the internal capsule and pyramidal tracts 
to their arborizations around the cells of the various intracranial motor 
nuclei and anterior spinal cornua. This is a compact segment and 
forms the pyramidal tracts. 

The lower motor segment consists also of a lot of neurones whose 



THE NEURONIC DISEASES 393 

cell-bodies are to be found in the anterior horns of the cord, while their 
axones pass out through the anterior spinal roots and related nerves 
to their termination in the distant muscles. 

The center of nutrition for each neurone resides in its cell-body. 
Therefore the tone and health of the upper neurones are dependent 
upon the integrity of the related cell bodies in the motor cortex ; the 
tone and health of the lower neurones are dependent upon the integrity 
of the related cell-bodies in the anterior horns of the cord. Each of 
these two sets of neurones exercise a nutritive control over the respec- 
tive structures below them and with which they are in physiological 
relationship. The tone and health of the lower neurones are to a con- 
siderable degree dependent upon the integrity of the related cerebral 
neurones ; the tone and health of the muscular tissues are very greatly 
dependent upon the integrity of the related spinal neurones. 

These facts have been all elucidated and illustrated in an earlier 
chapter. They are repeated here merely to show how a muscular 
atrophy of high degree may occur from a diseased condition in the cell 
bodies of the lower motor neurones ; and furthermore, to make plain 
how a lesser degree of muscular atrophy may occur from a disturbance 
of the health and functions of the lower neurones by a disturbance in 
the health and functions of the upper. 

Every muscular atrophy of neural origin is due to disease of the 
lower or peripheral neurones. This disease may be primary, in which 
case it is an original disease of the anterior gray matter of the cord ; 
or it may be secondary, in which case it is due to disease in the 
pyramidal tracts. This at once establishes two great types of spinal 
progressive muscular atrophy, the primary, or what Charcot used to 
call the protopathic type, and the secondary, or what he termed the 
deuteropathic type. As in both there must be always some disease of 
the lower motor neurones, many authorities do not recognize the dis- 
tinction between the two types just mentioned, but refer to them all 
as chronic muscular atrophy, progressive (central) muscular atrophy, 
spinal progressive multiple atrophy, spinal progressive amyotrophy. 

In view of the immediate pathogenesis of the muscular atrophy, 
this contention that they are all practically one and the same disease 
is a strong one. However, there are certain features in the clinical 
picture of the secondary, or deuteropathic, forms so unique and striking 
that it will perhaps be just as well to consider the latter in a section 
by themselves. I will discuss them under the head of amyotrophic 
lateral sclerosis. 

There is much better ground for separating the amyotrophic lateral 
sclerotic cases from those that are not of this type than there is for 
the separation of the latter into such subclasses as progressive bulbar 
palsy, progressive muscular atrophy and progressive hereditary muscu- 
lar atrophy; for these all represent pathologically the same disc 
with a symptomatology varied merely in accordance- with the gl 
anatomical location of the lesion; whereas tin- former represents a 
characteristic pathology that establishes a particular and distinctive 
clinical picture. 

Etiology. — In both the Aran-Duchenne type of i ve mus- 



394 



THE NEURONIC DISEASES 



cular atrophy now to be considered, and the Charcot amyotrophic lateral 
sclerotic type to be considered later, the immediate cause of the atrophy 
is, as was long ago shown by Levy and Lockhart Clarke, disease of the 
cells in the ventral horns of the cord. The cause of this disease is 
practically unknown, though Charcot believed that in amyotrophic 
lateral sclerosis it was secondary to disease in the pyramidal tracts. 
This is doubted to-day and even in Charcot's type the deterioration in 
the ventral horns is thought to be primary. 

Men are affected more frequently than women with progressive 
muscular atrophy. In most of the cases it appears between the ages 
of twenty-five and forty-five. A hereditary influence reveals itself in 
a small proportion of cases and in these it seems to be merely of a 
neuropathic character. In rare instances the heredity seems to be 
direct. In these cases several members of the same family may be 
afflicted and the disease occurs at an earlier age than usual. Such 
cases of a hereditary or familial type of progressive muscular atrophy 
of spinal origin have been observed by Werdnig, Hoffmann and others. 

The legs and back are first affected and later on the other muscles 
of the body. The disease advances slowly and terminates in the usual 
way, even with bulbar symptoms (Werdnig) in about four or five 
years. 

It is not yet positively established whether Charcot-Marie's type of 
hereditary muscular atrophy beginning in the leg is a central, spinal or 
peripheral neuritic malady. If it is the former, as Dana and others 
think, it would seem unnecessary to elevate it into a special affection 
and devote a separate section to its consideration. If it is a neuritic 
affection it would naturally fall into the chapter on neuritis. In my own 
opinion it is but a form of the disease we are now considering, and I 
will so describe it. 

The causes to which progressive atrophy have been attributed are 
so numerous that one instinctively doubts the reality of any of them. 
Nevertheless mention must be made of cold, dampness, exposure, men- 
tal strain, over-exertion, trauma, infection and intoxication. Perhaps 
the last two have a stronger claim for recognition than any. At all 
events the disease is said to have followed measles, typhoid fever, 
cholera, rheumatism, syphilis and childbirth. The atrophy of lead 
poisoning is not strictly of the progressive type. This disease has oc- 
curred as a senile form at the age of seventy. 

Pathology ano Pathogenesis. — A slow, non-inflammatory, de- 
generative process in the anterior horns of the spinal cord constitutes 
the primary pathological basis of the disease. Usually this is most 
marked in the lower cervical and upper dorsal regions. From these 
points it may extend upwards and downwards until the entire cord 
is involved. The large pyramidal cells, especially the central and me- 
dian groups, are shriveled and wasted, are greatly reduced in number, 
or are entirely absent. The neuroglia and connective tissue are in- 
creased ; but there are no distinctive vascular changes, though here and 
there a blood vessel may be dilated. The processes from the wasted cells 
are also atrophied where they pass through the white matter out into 
the anterior roots. Sometimes in the course of the disease, and to a lesser 



THE NEURONIC DISEASES 395 

degree usually, the white matter of the cord, particularly the pyramidal 
tracts, participates in the atrophic process. All parts of the lateral 
columns except the direct cerebellar and antero-lateral tracts, and also 
the antero-lateral ground bundle, may exhibit the atrophic condition. 
It was thought by Charcot that cases showing atrophy of the pyramidal 
tracts constituted a separate type of the disease, but in this he was in 
error, for many cases reveal upon post-mortem examination a consider- 
able atrophy of the pyramidal tracts, which during life manifested no 
spasticity, the symptom upon which Charcot largely founded his 
amyotrophic lateral sclerosis. The latter is only a clinical manifesta- 
tion of the general disease. In most of the cases there is sooner or 
later extension of the malady into the medulla. In some cases it seems 
to start and terminate in the medulla, constituting the type known as 
progressive bulbar paralysis. When the disease advances from the cord 
upwards, the homologous motor nuclei show the same general changes 
as do the anterior horns. Along the pyramidal tracts the degeneration 
lias been traced even as far up as the cerebral cortex. In the opposite 
direction the degenerative process has extended out through the anterior 
roots, into the peripheral nerves and even into the muscular tissue. In 
the latter the fibres are shrunken and diminished, their striations have 
disappeared, granulations and fat globules have taken their place and the 
interstitial connective tissue is increased. The entire muscle therefore 
is at first soft, then hard, and its appearance is pale, streaked and yel- 
lowish. Healthy fibres may continue here and there among the dis- 
eased ones and the small vessels among them may be dilated. 

A primary degeneration of the entire neuromuscular apparatus 
with its prominent focus in the anterior horns of the cord and their 
related structures, the muscles, constitutes the pathological basis of all 
forms of spinal progressive muscular atrophy. So uniform and con- 
stant, though not necessarily always to the same degree in all parts 
of this neuromuscular tract or apparatus, are these pathological changes 
found that were we to confine our attention solely to their anatomical 
side, all forms of progressive atrophy would be reduced to the nomen- 
clature of a single disease. 

Symptoms. — The moment we begin to attempt a classification of 
progressive muscular atrophy from its clinical presentations alone w< 
find that we must speak of different types, though in general the symp- 
tomatology of all types is about the same. If simple muscular atrophy. 
with a paralysis running along parallel with it, occurs without an\ 
other manifestation, we have the pure form of the disease. If spasticity 
accompanies the atrophy and paralysis, showing considerable involve- 
ment of the pyramidal tracts, we have Charcot's amyotrophic lateral 
sclerosis. If the simple muscular atrophy with paralysis appears firs! 
in particular groups of muscles, we have the Vran-Duchenne, the 
peroneal, the bulbar, tin ophthalmoplegic and other localized typ 

In all cases the disease develi ps slowly and insidiously. The 
tient may be affected for months and years, but not being particular!) 
discommoded, he either docs not notice the trouble or else fancies thai 
he is merely a little thinner than he oughl to be. I knew a case where 
the marked wasting of the upper limbs induced the pinna n r a long 



3 ( /> 



THE NEURONIC DISEASES 




FIGURE 67. 



1 FIGURE 68\ 



FIGURE 69. 



Fig. 67. — Chronic bulbar paralysis with amyotrophic lateral sclerosis. Section 
through the medulla. 

Fig. 68. — Amyotrophic lateral sclerosis. Section through the lower cervical 
cord. 

Fig. 69. — Spinal muscular atrophy. Section through the cervical cordL 
( St riimpcll -Jakob.) 



HE NEURONIC DISEASES 



397 



-time to the belief that she was generally run down and abnormally 
thin all over the body, though as an actual fact her lower limbs were 
plump and normal in size. 

The disease shows itself first in, and often remains limited to. the 
•upper extremities. Sometimes one limb is affected more than another. 

FIGURE 70. 




Progressive muscular atrophy. Age of patient forty five yean 

reich.) 



( After Fried 



In the beginning there may be some slight weakness and dull, rheuma 
toid pain in the muscles of the arm and shoulder; or there ma\ be a 
mild sort of rigidity causing the finer movements to reveal a traci 
awkwardness. Usually about this time the muscles have commenced 
to show some degree of wasting. In the more common Aran Duchenne 



39& THE NEURONIC DISEASES 

type the small muscles of the hand are the first to become atrophied. 
The balls of the thumb and of the little finger flatten ; the hollows be- 
tween the tendons on the back of the hand deepen ; the lumbricales and 
interossei seem to disappear and the fingers are scrawny and prominent 
at the joints. The entire hand gets flat and the thumb stretches parallel 
with the fingers, giving it the ape appearance. The adductor longus 
pollicis is soon involved. Adduction, abduction and flexion of the 
thumb is extremely difficult. Gradually the fingers are drawn back- 
ward and are abnormally flexed on account of the extension of the dis- 
ease up into the arm, thus giving them the well-known appearance of 
the main-en- griff e. As the disease advances on up the forearm, arm 
and shoulder it is noticed that the anatomical nerve distribution is not 
followed, although in many cases the ulnar nerve area is prominently 
involved. 

All possible changes are seen in the course of the disease. One arm 
may become far advanced before the other is attacked. On the other 
hand, the trouble may appear in the shoulder first, particularly the 
deltoid muscle, thence pass to the biceps, less frequently the triceps, and 
so on all the way down the limb. 

The appearance of the entire arm is very characteristic ; thin, 
wasted, with the grooves deepened, the bony prominences exaggerated „ 
it hangs limp and gaunt by the side. 

Other parts of the body beside the arms may be implicated. In 
fact, it is a peculiarity of the disease to thus skip about. The entire 
shoulder girdle may suffer and with it the deep muscles of the back. 
The legs are rarely affected, and then as a rule only late in life. The 
muscles of the pelvic girdle, particularly the glutei, the extensors and 
the abductors of the thigh, are occasionally attacked. The diaphragm 
becomes involved and ultimately the intercostals. Last of all the mus- 
cles of the neck and others under the control of the medulla succumb. 
Involvement of this important part of the brain usually brings the case 
to an early termination. Many years and almost an entire lifetime may 
be consumed by this slow progressing malady. 

Fibrillary twitching usually accompanies the advancing atrophy, 
together with paralysis. The electrical excitability shows a correspond- 
ing decrease. 

On account of the absence or presence of a slight rigidity and 
stiffness in the muscles two forms of the disease have been referred 
to — namely, the tonic and the atonic. These, as I have intimated before, 
are confusing and artificial distinctions. All that is necessary to note 
in regard to this is that in some cases the pyramidal tracts may be suffi- 
ciently implicated to provoke a mild degree of spasticity and give the 
case a resemblance to that still more pronounced, though arbitrarily 
separated clinical typo, amyotrophic lateral sclerosis. 

There are no objective sensory symptoms in progressive muscular 
atrophy and the subjective phenomena, like numbness and other mild 
paresthesia?, are infrequent and inconsequential. 

Some authors refer to other symptoms which are either of minor 
significance or indicate extension of the disease to the medulla. Such 
are sweating, local congestion and some other vasomotor troubles: 



THE NEURONIC DISEASES 399 

inequality of the pupils from irritation of the ciliospinal center ; weak- 
ened sexual power ; urinary abnormalities. 

There is a form of the disease, the Charcot-Marie peroneal type, 
in which heredity plays a striking role and the atrophy begins in the 
leg. It appears usually under twenty years of age. The trouble 
ascends, involving successively the peronei muscles, the extensors of 
the foot, the calf and ultimately the thigh. After many years even 
the upper extremity may be involved. The foot and hand frequently 
escape. Pains are complained of by many patients. This disease for 
the most part resembles an ordinary progressive atrophy. In other 
respects the type simulates an ascending neuritis. Hoffmann and 
others believed it was such and named it the neural type of progressive 
muscular atrophy. There are many good reasons for not regarding it 
as primarily neuritic in origin, but rather as poliomyelitic, like all the 
other spinal atrophies. A polyneuritis in which the foot and hand so 
uniformly escape would certainly be anomalous, and moreover heredity 
is not an influential factor in the production of peripheral nerve degen- 
erations. On the other hand, it is a fact that in all forms of progressive 
spinal atrophy more or less degeneration does occur in the peripheral 
nerves or outer ends of the diseased lower neurones. This would 
account for the diseased nerves observed in this type of the trouble by 
Yirchow, Friedreich and others. The other symptoms upon which 
the neural theory of the disease is based, as, for instance, the pains, are 
too insignificant to have much weight when placed in contrast with 
the many other manifestations which seem so strongly to ally it to the 
ordinary progressive muscular atrophy. The work of Dana, Marinesco 
and others has confirmed the belief that the primary cause of the 
peroneal type, as in all other forms of progressive atrophy, is a lesion 
of the anterior horns of the cord. 

De\gnosis. — In typical cases progressive muscular atrophy is easy 
of diagnosis if close attention be given to the onset, distribution and 
slow progress of the atrophy. Muscle groups rather than individual 
muscles or the whole limb is the predominant area of distribution. The 
atrophy precedes and, as it were, controls the paralysis. Sensory symp- 
toms are wanting except to a slight extent in the so-called neural, or 
Charcot-Marie peroneal type of the disease. A slight muscular stiff- 
ness and fibrillary twitching are -frequently present. The progress of 
the trouble is slow, skipping from muscle-group to muscle-group, often 
with temporary remissions, but always steadily onward. 

Clinically it is always wise to attempt a differential diagnosis be- 
tween progressive muscular atrophy, amyotrophic lateral sclerosis and 
chronic anterior poliomyelitis, though many authors insist upon refer- 
ring to all three as practically the one disease. 

In amyotrophic lateral sclerosis the marked spasticity with the com- 
paratively slight atrophy, the commencement of the trouble in the arms, 
and the bulbar manifestations, are all highly indicative-. 

In chronic anterior poliomyelitis the symptoms appear more sud- 
denly, reach a climax, and then recede, leaving a permanent paralysis 
in individual muscles. The paralysis always precedes the atrophy and 
is accompanied early, as a rule, by changes in the electrical reaction-. 



400 THE NEURONIC DISEASES 

At times it must be admitted the differential diagnosis is all but im- 
possible. In such cases time will show the slow extension of the atrophy 
to other muscles and parts of the body. When bulbar symptoms come 
on late to complicate the clinical picture the diagnosis of progressive 
muscular atrophy is assured. 

Other diseases from which a differential diagnosis may sometimes 
have to be made are the muscular dystrophies, peripheral neuritis, 
anthritic neuritis, cervical pachymeningitis hypertrophica, syringo- 
myelia, general gliosis, spinal caries and the occupation neuroses. 

From these progressive atrophy is best differentiated by exclusion. 
Each one has some characteristic symptom or symptoms that do not be- 
long to progressive atrophy and by this symptom the separation is made 
even though the atrophy, the paralysis and the course of the malady are 
the same. The heredity, the age of the patient, the prominent distribu- 
tion of the wasting and paralysis in the lower truncal and pelvic muscles, 
the leg and face, the existence of some hypertrophy or pseudo-hyper- 
trophy and the absence of stiffness and bulbar manifestations, indicate 
a muscular dystrophy. 

Multiple neuritis begins abruptly, spreads upward on the limbs 
and from the legs to the arms, exhibits ataxia, late atrophy, loss of the 
deep reflexes, electrical changes and marked local sensory phenomena, 
such as pain and hyp?esthesia 

Arthritic muscular atrophy is always in and around the diseased 
joint and does not extend to the entire limb or pick out special muscles 
or groups of muscles. The paralytic, electrical and reflex phenomena 
that accompany the classical form of muscular atrophy do not appear 
with the arthritic wasting. Moreover, the latter recovers rapidly after 
the joint trouble has disappeared. 

In the cervical hypertrophic type of pachymeningitis the symptoms 
seem to select the median and ulnar nerve areas for their manifesta- 
tion and there are the usual darting, radiating pains of posterior root 
irritation. The dissociation of the pain and touch sense, and the other 
trophic characteristics, besides the muscular atrophy, will help to 
determine the syringomyelia. 

Spinal caries is differentiated by the pressure symptoms, the 
meningitic pains and local tenderness, the spinal deformity and the use 
of skiagraphy. 

The history of overuse of a special set of muscles, the limitation 
of the trouble sharply to those muscles and its tendency to get well 
under simple rest, or at least its. indisposition to spread, points very 
clearly to an occupation neurosis. 

Prognosis. — Being a slow, progressive disease, the prognosis of 
muscular atrophy is bad so far as a cure is concerned. The lost neural 
elements, upon which the disease depends, cannot be restored by 
human power. The cases run on, however, for many years, sometimes 
remit and become stationary, or in a small percentage undergo what 
may be termed a partial recovery. The possibility of such nn event 
can be held out to the patient, but it dare not be promised or anticipated. 
The more symmetrical in distribution the atrophy is the better the hope 
for a partial recovery. The more marked the type of the disease is, 



THE NEURONIC DISEASES 4GI 

as, for instance, the hand, the leg or the amyotrophic, the more apt is 
it to be permanent. The condition met with at the end of six months or 
a year cannot be bettered in any way. Cessation at that point is the 
most than can be hoped for. The chances are that it will progress and 
extend. Death usually results from bulbar involvement, general ex- 
haustion and marasmus, or some intercurrent malady. 

Treatment. — It must be evident from the description of the nature 
of this disease that treatment is of little avail. Hygienic and symp- 
tomatic measures are about all that can be recommended. Over-exer- 
tion should be carefully guarded against and it is always wise to rec- 
ommend frequent and prolonged rest. All stimulants, general as well 
as local, alcohol, tobacco, sexual indulgence, cold baths, vigorous mas- 
sage, active or passive exercise and electricity had better be refrained 
from, or used very cautiously. Arsenic and thyroid extract may be 
tested, but they do not promise very much. Gowers. Sanger Brown 
and others have tried, with some degree of success, the subcutaneous 
daily injection of the nitrate of strychnia in doses of about 1-25 grain. 
The treatment may be kept up for six weeks, then stopped for two 
weeks, then renewed again, and so on until several courses are taken. 
It is a waste of time and money for a patient to seek new climates, hot 
springs and highly advertised sanataria in the hope of a cure. Rest, 
quiet and good nourishment at home, under the careful observation 
of his medical adviser, is the safest regime for his adoption. 

AMYOTROPHIC LATERAL SCLEROSIS. 

Our knowledge of this disease dates from Charcot's descriptions of 
it in 1869 and later. Other investigators have added much to this 
knowledge and cleared up some doubtful points in Charcot's original 
definition. 

Clinically the affection is revealed by a spastic paralysis with a 
distinct muscular atrophy and absence of sensory phenomena. Patho- 
logically it is a degenerative sclerosis of the upper and lower motor 
neurones. It is usually classed among the progressive muscular 
atrophies of spinal origin, because it exhibits all of the symptoms and 
post-mortem findings of these affections, in which the disease proi 
is located in the anterior horns, anterior roots, and their extensions out 
into the peripheral nerves. In addition to this, however, amyotrophic 
lateral sclerosis is a disease process in the lateral columns of the cord, 
especially the pyramidal tracts. Charcot believed that the degeneration 
of the pyramidal tracts was primary, causing a degeneration in the 
cells of the anterior horns and associated anterior root fibres secondarily. 
It is more probable, from the latest investigations, that the two pi 
esses, that in the pyramidal tract and that in the anterior horns, are 
merely coincident and are dependent upon the same cause. As the 
degeneration has been traced all the way up to the cortex, it is now 
the accepted opinion that amyotrophic lateral sclerosis is a degenerative 
disease of the entire motor path. 

Etiology.— We know very little about this. Heredity does not 
seem to enter as a factor, though it i> more than probable that a 1 



402 THE NEURONIC DISEASES 

genital neuropathic condition is responsible to a certain extent for its 
occurrence in certain individuals. It appears with about the same fre- 
quency in both sexes, though Charcot and Marie were of the opinion 
that females were more prone to it than males. It is a disease of mid- 
dle adult life. Most cases show themselves between the ages of thirty- 
five and forty-five, though they have been seen to occur at any time 
between the ages of sixty and thirty. Many exciting causes for the 
disease have been enumerated by the authorities, chief among which 
are exposure to wet and cold, mental strain, physical exhaustion, dissi- 
pation, sexual excesses, traumatism, etc. Syphilis does not seem to 
particularly predispose to the disease, but it has been observed in 
syphilitics. The etiology may well be summed up by saying that the 
predisposing cause, a neuropathic constitution, being present, almost 
any exciting cause in the way of a shock or intoxication may start the 
degenerative process in the motor path. 

Pathology and Pathogenesis. — The latest and most carefully 
made post-mortem examinations show that this disease is pathologically 
a degeneration of the entire cortico-muscular conducting path. The 
degeneration of the peripheral motor neurone is identical with that of 
the myelopathic form of progressive muscular atrophy. The anterior 
horns are the only part of the spinal gray matter that is degenerated. 
The pyramidal tracts, both crossed and uncrossed, reveal degeneration 
and the disease process has been traced up through the medullary motor 
paths, the peduncles of the brain, the internal capsule and even into the 
motor areas of the cortex. In the cord other structures have been found 
degenerated by Spiller, Mott, Probst and others, though these cases 
have been exceptional. The dorsomedian columns of Goll were wasted, 
likewise Clarke's columns and the direct cerebellar tracts. 

In the medulla the degeneration attacks the motor paths and the 
motor nuclei and the roots of the motor cranial nerves — namely, the 
hypoglossal, the facial, the vago-accessorius and the motor fifth. In 
one or two instances the nuclei of the ocular nerves have been im- 
plicated. 

In the brain the degeneration was observed in almost the entire 
motor cortex, the corpus callosum, the middle region of the posterior 
limb of the internal capsule, and the tangential fibres and the parts of 
the centrum ovale anatomically and physiologically connected with the 
cortical motor areas. The large pyramidal cells were diminished in 
number and the remainder were pigmented and atrophied. 

Spiller has detected a degeneration in the peripheral nerves even, 
side by side with undegenerated fibres. 

No degeneration was regularly found in any of the sensory paths, 
in the intramuscular nerve fibres or the muscle spindles. 

Symptoms. — The typical form of amyotrophic lateral sclerosis 
exhibits certain cardinal symptoms. These are spastic paralysis and 
atrophy in the upper extremities, and weakness and rigidity with slight 
atrophy in the lower; fibrillary tremor in some of the wasting muscles : 
exaggeration of the deep reflexes; more or less alteration of the elec- 
trical reactions; certain bulbar symptoms showing involvement of the 



THE NEURONIC DISEASES 403 

cranial nerves from the seventh to the twelfth ; and complete absence 
of all sensory and mental disturbances. 

There are types of the disease that vary slightly from this general 
clinical picture, according to the location and predominence of the 
lesion and the resulting preeminence of one or more groups of symp- 
toms. For example, in the majority of cases the trouble first shows 
itself in the upper extremities and later on in the lower, but there are 
rases in which the reverse order of events takes place. Occasionally a 
case will first announce itself by slight bulbar symptoms, a glosso- 
labio-laryngo-pharyngeal paralysis, the extremities not being implicated 
until later. 

In most of the cases spasticity and an exaggerated niyotatic re- 
sponse precede for a time the muscular wasting and even continue along 
with it pari passu. There are cases, however, where the disease in the 
lower motor neurones antedates for some time the disease in the 
pyramidal tracts, and having, for the time being, all the usual signs of 
a chronic poliomyelitis or even progressive muscuiar atrophy of the 
Aran-Duchenne type, cannot be distinguished from the latter diseases. 
It was for this reason, in a large measure, that Gowers, Leyden and 
even Charcot believed amyotrophic lateral sclerosis to be a mere form 
of spinal progressive atrophy, though the last author did subdivide the 
muscular atrophies of spinal origin into the primary or protopathic 
variety, in which the disease is limited to the lower motor segment, and 
the deuteropathic, or amyotrophic lateral sclerosis type, in which the 
disease is in both the lower and upper segments. In this latter type 
Charcot taught that the degeneration of the anterior cornua was a sec- 
ondary result of the degeneration of the pyramidal tracts. 

A cardinal symptom of amyotrophic lateral sclerosis is spasticity 
of the muscles. This appears before the atrophy, usually in the arms 
first, except in those very rare cases where the disease in the lower 
motor neurones has gone so far in advance of that in the pyramidal 
tracts that they cannot be differentiated clinically at all from Charcot's 
protopathic type. Even in those cases where the symptoms show them- 
selves first in the lower extremities there will be found upon careful 
examination a slight degree of rigidity, with weakness in the arms and 
hands. 

In all typical cases, therefore, of amyotrophic lateral sclerosis the 
arms will be observed to be strongly adducted, the forearm flexed, the 
hand pronated and the fingers more or less fixed in the claw position. 
In the legs the stiffness is shown in the walk. The patient steps slowly. 
more or less rigidly, and with short strides. Later on he seems only 
to be able to push himself along on the tips of his toes. This spasticity 
is the result of muscular tension, active contraction and atrophic 
paralysis. 

Equally important as tin- spasticity in the symptomatology 
amyotrophic lateral sclerosis, though not synchronous with it, is the 
progressive atrophy of the muscles. Individual muscles and groups 
muscles may be attacked, simultaneously or one after the other, accord- 
ing to the location and extent of the lesions, ft would be useless 
attempt to describe all of the types of atrophy that can appear in the 



404 THE NEURONIC DISEASES 

course of this affection. Suffice it to say that the wasting of the mus- 
cles, which usually is observed from a few months to many years even 
after the appearance of the spasticity, is never quite as marked as it is 
in the ordinary forms of anterior poliomyelitis or progressive muscular 
atrophy, and that furthermore it is more pronounced in the upper than 
in the lower extremities. In these it begins most frequently in the 
hand, gradually involving the shoulder and radial regions later. The 
muscles of the lips, the tongue, the jaw and the face may all become 

FIGURE 71 




Attitude of the hand in amyotrophic lateral sclerosis. (After Charcot.) 

stiff and atrophied. The trunk muscles, as a rule, escape or are not 
so profoundly implicated as are those of the extremities. In the final 
stages of the disease the diaphragm, the internal muscles of respira- 
tion, and even the visceral muscles may all become more or less affected. 

At an early period the deep reflexes are exaggerated, as, for exam- 
ple, those of the quadriceps, gastrocnemius, patella, Achilles, biceps, tri- 
ceps, scapular. A masseter clonus, elicited by gently tapping the edge 
of the lower jaw, was first studied by Beevor and Morris Lewis. The 
Babinski sign may be present, and later on contractures with threat- 
ening cardiac and respiratory phenomena. Early in the disease the 
electrical reactions are not far from the normal. As the atrophy ad- 
vances, however, the reflexes diminish correspondingly and the elec- 
trical phenomena assume irregularly the characteristics of the reaction 
of degeneration. 

At times a characteristic fibrillary tremor or twitching may appear 
in advance of the atrophy or it may even form the first objective symp- 
tom of the disease. 

The motor weakness that is present is not the result of the atrophy 
and contractures, but is an independent phenomenon. 

That amyotrophic lateral sclerosis is a disease of the efferent or 
motor path is clinically shown by the complete absence of all sensory 
Symptoms. In a few cases a slight paresthesia has been noticed. A 



THE NEURONIC DISEASES 405 

primary degeneration of the columns of Goll, with slight sensory phe- 
nomena, has been recorded by Hektoen ; and Mills has reported a case 
of associated tabes and amyotrophic lateral sclerosis. Such cases, while 
constituting the link between this disease and progressive muscular 
degeneration on the one hand, and locomotor ataxia on the other, should 
probably be looked upon as instances of combined sclerosis, rather than 
as examples of amyotrophic lateral sclerosis with a mere complication. 

Likewise there are no mental symptoms in this disease, though 
Spiller, Probst and Sarbo have recorded instances in which some mental 
disturbance was present. These were probably mixed cases and may 
well be accounted for by the wide extension, in a few individuals, of the 
degenerative process. 

Amyotrophic lateral sclerosis as a typical disease is therefore 
clinically a motor degenerative paralysis, and is characterized only by 
the symptoms spasticity, atrophy and paresis. 

Late in the disease, and usually as its terminal phenomena, bulbar 
paralysis occurs. Dysarthria proceeds to anarthria. Deglutition be- 
comes difficult and even impossible. The lips, the tongue, the palate 
and the cheeks are paralyzed, atrophied and electrically altered. Drool- 
ing from the mouth occurs, the speech is blurred and 'Tailing" in 
character, and aphonia supervenes. Finally after the disease has run 
its course in from two to four years, the end comes as the result of 
inanition, asphyxia or aspiration pneumonia. 

Diagnosis. — A typical case of amyotrophic lateral sclerosis is not 
hard to diagnose, for it presents a strikingly characteristic group of 
symptoms — namely, spasticity, paresis, atrophy and absence of all sen- 
sory and mental phenomena. When the disease process in the peripheral 
motor spino-muscular system precedes for some time the disease 
process in the central cortico-pyramidal system, it may be impossible to 
differentiate it clinically from the myelopathic type of progressive mus- 
cular atrophy. In such cases, however, some slight degree of spasticity 
can be detected upon careful examination in some muscles later on that 
have escaped the first onset of the malady. Cases in which other de- 
generations are associated with those of the amyotrophic may give 
much trouble in the diagnosis. A most careful weighing and compar- 
ing of the various symptoms of the associated affection with those oi 
Charcot's disease can alone render a differentiation at all possible. 
Bearing in mind the characteristic traits referred to elsewhere, amyo- 
trophic lateral sclerosis, with its peculiar features, ought not to cause 
much trouble in differentiating it from progressive muscular atrophy, 
bulbar and spinal chronic poliomyelitis, syringomyelia, focal spinal 
pachymeningitis or cervical hypertrophic pachymeningitis, multiple 
neuritis, the cortical encephalitis of Strumpell, disseminated sclerosis. 
the muscular dystrophies or diffuse myositis. 

Prognosis. — This is bad, as the disease invariably terminates 
fatally in a few years. 

Treatment. — The treatment is limited and unsatisfactory. Tonics. 
fresh air and good nutrition should, of course, be given. Though 
Gowers recommends injections of strychnine, and others have suggi 
electricity, a trial of the je measures has not seemed to materially modify 



406 THE NEURONIC DISEASES 

the course or termination of this progressive and profound degenera- 
tion. 

PROGRESSIVE BULBAR PARALYSIS. 

This disease was first described by Duchenne in i860, and ten 
years later its lesion was accurately located by Charcot and Leyden. 
It is sometimes called progressive glosso-labio-laryngeal paralysis. 

It is a primary, degenerative disease of the bulbar cranial nerves 
of motion. These nerves are the analogues of the spinal motor 
nerves, and their nuclei in the floor of the fourth ventricle are the 
homologues of the anterior horns of the cord. This form of progres- 
sive, primary degeneration in them, therefore ; is nothing more nor less 
than another view of progressive muscular atrophy. That this is so 
is further proved by the fact that on the one hand bulbar paralysis 
almost constantly appears sooner or later in the poliomyelitic type of 
progressive muscular atrophy and the amyotrophic type, and on the 
other hand degeneration in the pyramidal tracts and in the spinal an- 
terior horns is almost invariably found in the late cases of this dis- 
ease. In other words glosso-labio-laryngeal paralysis of the progres- 
sive type is progressive muscular atrophy prominently appearing in the 
medulla oblongata. For this reason I classify and describe it here 
rather than under the head of diseases of the medulla. It is not a dis- 
ease of the medulla in the true sense of the word. It is merely a phase, 
a unique manifestation, of progressive muscular atrophy. The symp- 
tomatology of it may suggest an independent classification, but its 
pathology binds it down as one of the unique localization types merely 
of the general disease of the entire motor tract known as progressive 
muscular atrophy. Only in symptomatology therefore does bulbar 
paralysis of the progressive type stand forth independently. 

Etiology. — What has been said of the etiology of the two pre- 
ceding affections is strictly applicable here, for all three diseases are 
one and the same. 

It is rare and occurs mostly in late adult life. It is all but un- 
known before the fortieth year of age. In a few instances it has been 
reported as having occurred in children, though there is some doubt 
about the exact pathological similarity of these cases with the typical 
disease. I do not regard the infantile hereditary and familial types 
of progressive bulbar paralysis as corresponding exactly with the type 
now under consideration. They are more strictly bulbar diseases, con- 
genital nuclear atrophies, and not a mere part of a general progres- 
sive motor atrophy. They will be referred to again under the head of 
diseases of the lower motor segment more particularly. 

As in the other manifestations of the disease, a neuropathic tend- 
ency is here present, responding to such exciting causes as cold, exces- 
sive emotion, shock, traumata and over-exertion of the muscles, such 
as those of the lips, tongue or larynx, that are innervated by the me- 
dulla. 

Pathology and Pathogenesis.— To describe this I would but 
have to repeal what 1 have said under the head of progressive muscu- 



THE NEURONIC DISEASE! 



407 



lar atrophy. The changes are the same, but in this instance they have 
started first in the nuclei of the motor cranial nerves, namely, the 
facial, the motor branches of the glosso-pharyngeal and vagus and 
the hypoglossal. The spinal accesssory, of course, is a spinal nerve in 
reality so that it escapes in bulbar paralysis, and the limited nosol- 
ogy does not include implication of the ocular motor nuclei. The motor 
branch of the fifth nerve is occasionally included in the disease process. 
The pyramidal tracts may atrophy in some cases before the gray nu- 
clei, or accompany it or be entirely absent. The same is to be said 
of the degeneration in the anterior horns of the cord. 

Symptoms. — It is due almost entirely to its symptomatology that 
progressive bulbar paralysis owes its distinction as a separate sort of a 

FIGURE 72. 




Normal hypoglossal nucleus. Atrophic hypoglossal nucleus in bulbar 

paralysis, g, blood-vessel. 

(After Oppenheim.) 

disease. A progressive, atrophic paralysis involving both sides oi the 
face and destroying the speech, the deglutition, the phonation and the 
mastication constitutes the sum total of the clinical manifestations of 
the disease. 

Usually the speech is the first function to be affected. Words and 
sentences with many dentals and Unguals and linguo-palatal letters in 
them arc- hard to utter and soon tire the patient. He cannot close 
the lips as tightly as he should to utter the explosives p and 1). ( In 
account of the added nasal tone, he sounds these letters as it" they were 
nip or nib. To say smoothly the sentence. "Peter Piper Picked a Peck 
of Pickled Peppers/' or "Round the Ru{ ck the Ragged Ras 

cal Ran," is almost impossible. Dysarthria with a nasal twang is thus 
an early and characteristic manifestation. There is a suggestion in the 
speech as if something were in the month, so much so thai a mother 
in a certain case constantly asked her daughter for a long time to take 
what she had in her mouth out before she addressed her, much to the 
annoyance of the daughter, who of course, had to regularly deny the 
allegation. Exhaustion increases the speech difficulty. 



408 THE NEURONIC DISEASES 

Next the tongue is seen to be paralyzed. It rests limp, shriveled 
and immovable on the floor of the mouth. The mucous membrane 
on it is thrown into folds. At first there are marked fibrillary twitch- 
ings and tremors in its muscle. The lingual muscles are markedly 
atrophied. On account of all this the food bolus cannot be pushed 
back into the pharynx and deglutition thus becomes positively im- 
paired. There is regurgitation of fluids up into the nostrils and down 
into the larynx. This of course provokes choking and coughing. The 
saliva accumulates and drools out of the mouth over the edges of the 
paralyzed lips. Vomiting not infrequently occurs as a result of the 
disturbances of and efforts in swallowing. At length there is com- 
plete aphagia, or inability to swallow any solid or fluid. 

Later on in the disease mastication is difficult and sometimes im- 
possible. 

The involvement of the laryngeal muscles eventuates in first 
dysphonia and finally aphonia, the respiration suffering at the same 
time. There is in the early stages a weakening, a softening, a monot- 
ony o<f the voice. Choking spells, coughing, shortness of breath, and 
towards the end alarming and distressing dyspnoea are observed. The 
laryngeal paralysis is not usually as severe as that of the lips and tongue 

The movements of all the muscles of the various functions just re- 
ferred to are gradually and slowly restricted. The muscles themselves 
are also distinctly degenerated. This and the fibrillary tremor and 
the electrical reaction of degeneration are all characteristic of progres- 
sive atrophy. The reflexes, notably the jaw and pharyngeal, are abol- 
ished. 

The facial expression, as may well be imagined from this descrip- 
tion of the limitation of movements and muscular wasting, is unique. 
The folds are shallow or wanting, the mouth stands partially open, 
the lower lip hangs down and the saliva drools over it. There is a 
fixed, expressionless countenance, a sort of dead, listless, waxy ap- 
pearance. All of this involves mostly the lower half of the face, the 
upper half being comparatively intact and showing by its greater 
mobility the retention of the patient's mental activities. This relative 
freedom of the upper part of the face distinguishes this form of bul- 
bar paralysis, in part, from the infantile form where the brow cannot 
be corrugated nor the eyes tightly closed. 

Naturally this condition would cause a high degree of emotion- 
alism in these patients, but this emotionalism is to a certain extent a 
symptom and not a mere sequel of the disease. It is a part of the neu- 
ropathic complex and enters into its clinical presentation. 

With what has already been said in regard to this disease being 
but progressive muscular atrophy in a particular part of the motor 
tract, it hardly needs to be repeated that there are absolutely no sen- 
sory symptoms. Furthermore it is to be expected that in some cases, 
as in the amyotrophic types, there will be a certain degree of spasticity 
of the muscles and an exaggerated condition of the reflexes. Spinal 
manifestations of the disease may also appear in conjunction with, or 
later than, the bulbar symptoms. Thus the arm* iM hands may ex- 
hibit the atrophic paralysis. 



THE NEURONIC DISEASES 4O9 

Diagnosis. — If the symptoms of this disease be closely watched, 
there ought to be very little chance of a mistake in diagnosing- it. In 
the early or beginning paralysis, a lesion of the lower motor cortex 
might be thought of by mistake. In bulbar palsy the symptoms are 
always bilateral, whereas in cerebral trouble they are rarely so. Atrophy 
occurs in the former, not in the latter. Polioencephalitis is somewhat 
more acute and less progressive in its symptomatology than is this 
disease. There are acute bulbar paralyses that sometimes offer con- 
siderable confusion. The reader is referred to them in the section on 
diseases of the medulla oblongata. Medullary tumor is accompanied 
by the usual pressure symptoms of all intracranial growths, does not 
produce bilateral symptoms, nor does it pick out the nuclei and limit 
its effects to them and their nerves as does this disease. 

A careful distinction must be made between this type of progres- 
sive bulbar paralysis and the hereditary or familial type spoken of 
under the head of diseases of the medulla. The latter occurs always 
in children in whom there is a degenerative heredity. Consanguinity 
in the parentage is sometimes in the history. The child exhibits mark- 
ed stigmata of degeneracy. The atrophic paralysis begins in the upper 
part of the face and continues there during the involvement of the 
lower part. Ptosis is present. The ocular muscles are usually in- 
volved. There are no signs of atrophic paralysis in the extremities 
or trunk. The facial expression is that of dementia. Death occurs 
usually in two or three years. The cases are rather hereditary develop- 
mental anomalies, closely related, in some of them at least, to the facial 
and oculomotor diplegias. 

Prognosis. — Bulbar paralysis is a fatal disease, ending always 
in death after two or three years, rarely more. It is caused by the 
respiratory disturbance as a rule which appears in the form of an as- 
piration pneumonia, or an asphyxia. Inanition also is present. It is 
the appearance of bulbar symptoms that often foretells the early de- 
mise of the victims of the other forms of progressive muscular atrophy. 
Very rarely the disease runs on several years, slow and progressive, 
but with remissions. 

Treatment. — The disease is incurable and the treatment there- 
fore useless. Nitrate of silver, strychnine, arsenic, potassium iodide 
and galvanism are all suggested. I have never heard of any case be- 
ing modified for the better by any of these. 

Symptomatic treatment may be called for. Thus the drooling of 
the saliva can be checked somewhat by the restriction of its secretion 
with the administration of atropine. The patient's nourishment may 
have to be kept up by artificial feeding through a stomach tube-. There 
are no prophylactic measures to be recommended, because we do not 
know why the disease appears. 

PROGRESSIVE MUSCULAR DYSTROPHY. 

The muscular dystrophies, Erb's dystrophia muscularis pro, 
siva, are related clinically to the progressive muscular atrophies. They 
are not nervous affections and strictly ought not to be considered in 



410 THE NEURONIC DISEASES 

a work of this sort. They are primary diseases of the muscular tis- 
sues and are largely the result of heredity and developmental defects. 
It will not be amiss, however, to consider them here, for their clin- 
ical presentation is in many respects so like the spinal atrophies that 
for diagnostic purposes, and until our knowledge is more exact, they 
can be placed side by side. 

Many histologists and physiologists take the broad view that the 
lower neurone and its related muscle is a single mechanism, a uni- 
form, composite organ, and that disease of the neural or muscular part 
of this apparatus is merely a question of location and not of essential 
pathology. Neural disease affects the muscles ; the muscle disease re- 
acts upon the neural tissue. For aught we know positively the latter 
may be due to some minute form of neural trouble, cellular, mole- 
cular or physio-chemical, too fine for our coarse means of investigation. 
As heredity always plays its most brilliant role in connection with the 
nervous system and as it is such an important factor in the muscular 
dystrophies, the last suggestion is not such an illogical one. 

Clinically these diseases have been divided into separate types, 
though it must be kept in mind that etiologically and pathologically 
they are all the same. The types are founded upon the age of the 
patient, the muscles attacked, the presence of hypertrophy or pseudo- 
hypertrophy and the prominence of the heredity. Erb makes two grand 
divisions of them into, 

I. The infantile cases (dystrophia muscularis progressiva infan- 
tum), and 

II. The cases that occur in youths and adults (dystrophia mus- 
cularis progressiva juvenum vel adult orum) . 

Class I. is further subdivided into the hypertrophic and atrophic 
forms. Of these the hypertrophic cases may be truly hypertrophic or 
only pseudo-hypertrophic , while the atrophic cases may begin with 
primary involvement of the face or without involvement of the face. 

The shaded figures illustrate roughly the early localization of these 
various types. After discussing the main features of progressive mus- 
cular dystrophy, the clinical types that have been recognized will, un- 
der the same head, receive brief notice. 

Etiology. — The first thing preeminently obvious in the etiology 
of the muscular dystrophies is the influence of heredity. The trouble 
is not merely congenital, but genuinely hereditary. The influence is 
transmitted through the mother and is often pure and direct. The 
ovum carries the impress which it obtains from being a part of her 
own constitution. Its further development is affected by this im- 
press. Therefore it is that the muscular deterioration, which may not 
begin to show itself in the child until the end of the first or the middle 
of the second decennial period of life, is the result of a developmental 
defect and not of an acquired disease. The mother usually exhibits 
the same disease as her child. Brasch saw a case in which the mother, 
forty-two years of age, developed, after the birth of her dystrophic 
child, a hypertrophic form of the trouble. 

In some cases a marked new -opaline tendency is traced in the 
maternal ancestry. Syphilis, alcoholism, consanguinity do not seem 



THE NEURONIC DISEASES 41 1 

to be of any great significance. What the impulse is, or how far back 
in the ancestry it began, we are totally ignorant of. Some authors men- 
tion traumata and acute diseases as provocative causes. Boys are 
jnore frequently affected than girls, and most of the cases begin be- 
fore the age of ten. 

Heredity then is the one great factor that distinguishes the etiology 
•of these muscular anomalies. The age and sex are probably mere sub- 
sidiary factors. 

Pathology and Pathogenesis. — The essential element in the 
pathology is a change in the muscular tissues, primary in origin and 
nature, whereby a hypertrophy alternates with an atrophy. The change 
is clearly due to an inherent developmental weakness in the muscular 
■elements themselves and seems to select first those muscles generally 
that were the latest to have developed embrvologically. The biological 
importance of the latter fact, as indicating the hereditary developmental 
nature of the trouble, can hardly be over-estimated. 

All the muscles are not equally attacked in the same way. This 
-constitutes the misleading basis upon which the various types of the 
disease have been erected. The legs especially seem to be the loca- 
tion for the changes to be especially marked in ; next the muscles of the 
pelvic girdle and lower part of the trunk ; and lastly those of the face, 
shoulder and arm. On account of the hypertrophic condition in some 
muscles and the atrophic in others the general contour of the part is 
greatly altered. Sometimes a part of a muscle may be so enlarged as 
to produce a remarkable intumescent or tumor-like appearance. In 
one case I saw the calves so excessively enlarged that the appearance 
■of the patient, when standing, was positively ludicrous. The outline 
of the altered tissue is quite sharp in most cases ; in others it fades 
away into the normal tissue. 

There are reasons for suspecting that the changes in the mus- 
cles undergo a more or less regular and uniform process. There are 
-early signs of irritation such as swelling of the muscle fibre, prolifera- 
tion of the nuclei and connective tissue and splitting and breaking up of 
the muscular strands. The areolar and connective tissues undergo hy- 
pertrophy and the muscular fibres become actually hypertrophied. This 
of course enlarges the entire muscle mass. Gradually, however, the 
true muscle fibres waste, diminish and disappear. The associated tis- 
sues do not waste. In this way the muscle mass remains enlarged 
while the true muscle tissue is actually diminished. Tins is the pseudo- 
hypertrophic condition so characteristic of the dystrophies. Fatty de- 
posits occur in the muscles and even vacuoles are formed. As the 
muscular fibres continue to diminish and disappear and the connec 
tive tissue increases and fills in the vacancy, the muscle becomes hard 
and dense. It assumes a condition of myosclerosis, Vfter a long time 
nothing is to be seen but dense connective tissue and atrophied fib 
With all this change in the muscles, the nerves and spinal cord 
main normal. In some cases secondar) changes have been observed 
of a neuritic and poliomvelitic character. 

It would be rash to affirm thai these dystrophies are in any way 
directly dependent upon neural changes. In the present state <>f our 



4T2 



THE NEURONIC DISEASES 



FIGURE 73- 




Juvenile 'y]' e 



T /f e 



Muscular atrophy. 



THE NEURONIC DISEASES 



413 



FIGURE 74. 



/Arwyolrovh 

J rp ' 

'/r e 



T yr c 




Muscular atrophy. 



414 



THE NEURONIC DISEASES 






bo 







THE NEURONIC DISEASES 



415 



knowledge we must be content to regard them as primary, develop- 
mental defects in the muscular elements. And yet when the sym- 
metrical distribution, which not infrequently obtains, is taken into ac- 
count, when it is remembered that in many cases neural changes are 
observed which cannot positively be asserted to be always secondary 
to the muscular changes, and when finally the close biological and 
physiological relation between the nervous and muscular apparatuses 
is considered, it is not so unreasonable a suspicion to hold that even 
the muscular dystrophies may be due to some minute physio-chemical 
nutritive disturbance in the spinal nerve cells, which our present means 



FIGURE 78. 



FIGURE 79. 




Pseudo-hypertrophic paralysis. (After Duchennc. ) 



of research cannot detect, but which may be the immediate cause of 
the muscular deterioration. This of course is only a conjecture and 
must not yet be assumed as true. It is so much more desirable a 
hypothesis in accounting for the many similarities between the inns 
cular dystrophies and the progressive muscular atrophies than is the 
hypothesis of a primary muscular degeneration in accounting for their 
few differences, that it is worthy of much consideration and if pos- 
sible of future establishment by positive proof and demonstration. 

Symptoms. — Instead of symptoms, one might truthfully say that 
the symptom of this disease is hypertrophy or atrophy of the muscles. 
All muscles of the body may be affected, though the change appears 



4i6 



THE NEURONIC DISEASES 



more frequently in some than in others. Both hypertrophy and atrophy 
may appear simultaneously in different, and even in distant, muscles, 
or in different parts of the same muscle. There is no rule about the 
matter and the pathology cannot be made a basis for the separation 
of the malady into types. On account of these muscular alterations 
certain forms of paralyses occur, deformities appear, and alterations in 
the bodily movements take place. There are no distinctive sensory 
symptoms. 

With the atrophy a parallel paralysis, loss of reflex action and 
slight electrical changes take place, but none of these are as pronounced 

FIGURE 80. 






Attitudes assumed in pseudohypertrophic paralysis during attempts to rise. 
(Gowers.) 

or characteristic as they are in the true neural atrophies. Coldness, 
discoloration and other general vasomotor disturbances are liable to 
appear in the affected limbs. The general nutrition remains normal. 
The sphincters continue active. The sexual function is diminished or 
lost. The mind remains clear. 

I will now briefly consider the varieties of the disease that have 
been artificially established on the basis of the particular distribution of 
the predominant symptom. In doing so I will at the same time be giv- 
ing a more or less complete clinical picture of the entire affection. 

Pseudohypertrophic Muscular Paralysis (Muscular Pseudo-hyper- 
trophy; Lipomatous Muscular Atrophy). In this form of the disease 
there appears in the child usually a weakness, followed by enlargement 
of the calves of the legs. A peculiar waddling gait is thus noticed 
and there is some difficulty experienced in climbing the stairs. Some- 
times the child falls unexpectedly, and has considerable difficulty in 



THE NEURONIC DISEASES 



417 



getting up. It is noticed that when laid upon his back on the floor he 
first rolls over on his face, draws himself together, keeping his hands 
and knees upon the floor, and then with a hand on each of his legs 
climbs up upon himself, sliding his hands, and grasping his legs one 
after the other at successive levels, until he has attained the erect 
position. This manceuvre in getting up is so characteristic that it is 
almost pathognomonic. It is well illustrated in the accompanying pic- 
tures from Gowers. As the disease progresses the extensors of the leg 
and the flexors of the thigh become so weak that the attitude grows 
characteristic. The spine sags forward with a marked concavity open- 
ing backwards. This lordosis is always seen when the patient is stand- 

FIGURE 81. 




Progressive myopathy. Advanced case with marked Lordosis in >ittin.u. 
Souques-Brissaud.) 



(After 



ing and sometimes when seated. In certain mild cases it may disappear 
in the sitting posture. It is a feature of tin- lumbar part of the spine 
and causes a marked protrusion of the abdomen forwards and <>t" the 
shoulders backwards At this Stage of the disease the legs are usually 
enlarged, ofttimes remarkably so, and are barrel-shaped. The muscles 
about the hips and in the lumbar region exhibit considerable atroph) 
with here and there a curious lipomatous-like swelling. The from of 
the thigh has bulged in this way and one hi]) has been more prominent 

than tile Other. After tile teg and lumbar muscles, perhaps the shi 
der and upper arm muscles, are the mOS( frequently implicated, 
infraspinatus the deltoid, the lower part of the trapezius, the pert. • 
major, the serratus anticus major, the rhomboids, the biceps, the brachi- 



418 THE NEURONIC DISEASES 

alis internus and the supinator longus may all or any one of them be 
weak and paralytic. Alternations of hypertrophy and atrophy may be 
observed in them. The attitude and movements of the shoulders, the 
elevation of the arms, and the stationary position of the scapulae are 
all distinctive. In the lower part of the body the glutei, the latissimus 
dorsi, the quadriceps femoris, the adductors, the calf and peroneal mus- 
cles exhibit the characteristic change and debility. The tongue in rare 
instances is hypertrophied. The distal parts of the extremities, par- 
ticularly the forearms, the neck and face, are rarely included in the 
disease process. 

Thus we note that pseudo-hypertrophic paralysis is a widespread 
affection, though the changes in the leg muscles and the gait are the 
most constant and obtrusive symptoms. 

In the Juvenile type of Erb, the scapula-humeral form of the dis- 
ease, the dystrophy, as its latter name indicates, is most prominent at 
first in the muscles that make up the shoulder girdle. The same gen- 
eral process takes place that has already been described for all forms of 
the disease. Gradually it extends down the arm and very late in the 
course implicates the forearm and the legs. The beginning of the case 
is the only feature in which it differs from the other types. As it is 
slow and progressive it ultimately comes to have all the general quali- 
ties in regard to the muscular hypertrophy and atrophy, the gait, and 
the curvature of the spine that they have. 

The Facio-Scapulo-Humeral type of Landouzy and Dejerine is 
often spoken of as the infantile form because it so often appears earlier 
than the others. It may, however, show itself at the same age. The 
implication of the face with the shoulder and arm is its dominant trait. 
The weakness and wasting are particularly observable in the orbicularis 
palpebrarum and the orbicularis oris, so that the eyes cannot be closed 
completely and the lips protrude tapir-like. The involvement of the 
buccinators causes difficulty in eating and chewing, and a puffing of the 
cheeks in talking. The disease of the risorius and zygomaticus major 
renders smiling all but impossible. As the face in these cases is usu- 
ally where the trouble manifests itself first, the patients not infrequently 
declare that from early childhood they have been told by their friends 
that they never smiled or closed their eyes as they should. So slow and 
insidious is the extension of the disease down into the shoulder girdle 
that many of its victims fatuously imagine' they are merely constitu- 
tionally thin. Ultimately these cases, like those of the other types, 
develop the same general appearances in other parts of the body. 

The myopathic face with non-implication of the ocular muscles or 
the muscles of mastication and deglutition, and the prominence of the 
atrophy in the shoulder and arm, is the sign-manual of this infantile 
form of muscular dystrophy. 

There is a markedly hereditary form in which the symptoms begin 
in the lower part of the back and legs. It is not sufficiently unique, 
however, clinically or pathologically, though it is slightly so etiologi- 
cally, to warrant its further detailed description. 

Diagnosis. — As our knowledge will increase, it is not improbable 
that these muscular dystrophies will be seen to be closely related to, 



I 



THE NEURONIC DISEASES 



419 



FIGURE 82. 




Muscular atrophy. 



420 THE NEURONIC DISEASE9 

if not identical with, the progressive muscular atrophies. For the 
present, however, it is safe and convenient to recognize a distinction 
between the two, for in a general way the dystrophies possess certain 
preeminent traits apart from those of the progressive spinal atrophies. 
They may be roughly enumerated as pronounced heredity, early onset 
of the symptoms, a peculiar and characteristic distribution of the mus- 
cular changes, the simultaneous association of atrophy, hypertrophy 
and pseudo-hypertrophy , an absence of fibrillary twitchings and of the 
electrical reactions of degeneration. 

Many of the dystrophies do not conform absolutely to all of these 
requirements, while, on the other hand, occasionally a case of pro- 
gressive muscular atrophy assumes a remarkable likeness to a dystrophy. 
These enumerated traits, nevertheless, are important in aiding in the 
drawing of the distinction. 

There are a number of diseases in which muscular atrophy occurs 
which must not be confused with the trouble now under consideration. 
Chief among them are multiple neuritis, anterior poliomyelitis, pro- 
gressive muscular atrophy and cerebral atrophy. 

In multiple neuritis the abrupt onset of the malady, its rise to a 
climax and its tendency to subside, the marked sensory phenomena, the 
ataxia, the disproportion between the paralysis and the atrophy, the 
absence of heredity with the presence of infection or intoxication, will 
readily enable one to make the correct differential diagnosis. 

Anterior poliomyelitis exhibits more or less febrile phenomena, is 
acute or subacute, is not progressive, but rather regressive up to a 
certain point, and is devoid of practically all of the distinguishing traits, 
except perhaps the atrophy of the dystrophies. Moreover the electrical 
reactions are marked in poliomyelitis. 

The cerebral atrophies are not typical as are the spinal or the dys- 
trophic. They are monoplegic or hemiplegic in distribution, are pre- 
ceded by the paralysis, possess all the usual signs of hemiplegic de- 
generation of the upper motor tract, and are notably wanting in the 
characteristic traits and mode of development of the dystrophies. 
Hysteria, epilepsy, idiocy, tabes and poliomyelitis may complicate a 
dystrophy and so render the diagnosis difficult, especially if the appear- 
ance of the muscles is not very different from the normal, on account 
of the nice balance between the atrophy and the hypertrophy. 

Prognosis. — The course of the disease is apt to be a prolonged 
one, with periods of quiescence and even of remission. In the late cases, 
such as occur among the juvenile types, there may even be partial re- 
covery. Once started, the disease never disappears. Most of the 
patients die young from implication of the muscles concerned directly 
in the maintenance of the vital processes, as, for instance, the dia- 
phragm ; also from general marasmus and intercurrent affections. 

Treatment. — The treatment is of no avail. General hygienic and 
symptomatic measures exhaust the entire theme. Exercises must be 
moderate and the mechanical treatment with baths, electricity and 
massage must be undertaken very cautiously and tentatively. Tenotomy 
and other orthopaedic measures may lighten the existence of some of 
these patients. 



THE NEURONIC DISEASES 42 1 

b. DISEASES OF THE UPPER MOTOR SEGMENT. 

SPASTIC PARAPLEGIA OF ADULTS. 

For our knowledge of this affection we are indebted chiefly to 
Seguin, Erb and Charcot. They named it respectively tetanoid para- 
plegia, spasmodic spinal paralysis and spasmodic dorsal tabes. It is 
better identified clinically than it is pathologically. While much differ- 
ence of opinion still exists, it will nevertheless be well to recognize 
it as a clinical entity and to await further data in regard to its exact 
pathology. 

There is an infantile and an adult form of the disease. Most of the 
infantile cases, commonly referred to as Little's disease, are really not 
paraplegic, but hemiplegic. They are cerebral double hemiplegias, or 
cerebral diplegias due to vascular disease and will be found discussed 
under the . head of extra-neuronic brain diseases. A pure, primary 
spastic paralysis of spinal origin in childhood is a great rarity, if it oc- 
curs at all. Van Gehuchten, Souques, Raymond, Erb and Dejerine all 
believe that it does exist. 

Questionable as are the adult and infantile forms of pure primary 
spinal spastic paralysis, still more questionable are the hereditary forms. 
The assumption is made in regard to all forms that there is a degen- 
erative sclerosis limited entirely to the pyramidal Irwts. In a large 
number of cases both the clinical and pathological evidence is not- 
wanting, some time or other, to show that the lesion is not so well de- 
fined. The elasticity of the name lateral sclerosis, which is occasionally 
employed to designate the disease, gives it an advantage over spastic 
spinal paralysis, which represents only one symptom and presupposes a 
narrow and doubtful pathology. 

Etiology. — The cause of this disease is obscure. This applies to 
the hereditary as well as to the acquired forms. In the hereditary form 
several members of a family may be attacked and the symptoms first 
appear at about the age of five. Nothing is known as to the condition 
of the ancestry in these cases. It is not improbable that in the acquired 
forms there may be a slight neuropathic heredity, whereby certain 
neurones are rendered less able to resist active influences of a deleteri- 
ous sort. These cases are first observed between the ages of twenty 
and forty, and in the majority of instances follow sonic sort of intoxi- 
cation. Syphilis has been credited. I have considered thi> syphilitic 
form of the disease under the head of spinal syphilis and have there 
stated my doubt as to its existence. Trauma was thought to have- been 
the cause in some cases. From the etiological as well as from the 
pathological side, the more extensive character of the disease than 
what is assumed in the mere sclerosis of the pyramidal tracts is hinted 
at; for while most cases reveal upon post-mortem examination ap- 
pearances that suggest secondary degeneration from transverse 
myelitis, multiple sclerosis, or cerebral disease, thes< conditions are 
just the ones to be initiated by the etiological factors to which spinal 
spastic paralysis is frequently attributed— namely, trauma, the puer- 
perium, the infection.-, lead intoxication, poisoning from different 



422 



THE NEURONIC DISEASES 



forms of lathy rus, etc. Westphal was of the opinion that only in 
dementia paralytica did such a strictly limited primary sclerosis of the 
pyramidal tracts ever occur as is assumed in this disease. 

From the little that we know as yet in regard to its etiology, 
spastic spinal paralysis in its pure form is probably a result of a 
general agenesis and therefore is more or less hereditary; or it is the 
residual secondary degeneration from other and more diffuse diseases 
of the brain and spinal cord. In a word, the etiology such as we know 
it to-day does not favor the view that spastic spinal sclerosis is a limit- 
ed primary degenerative sclerosis of the pyramidal tracts. 

Pathology and Pathogenesis. — Not much need be said on this 
score, since we know so little positively. Elsewhere I have shown that 
the degeneration of the pyramidal tracts noted in Little's type of spastic 
paralysis is a double hemiplegia and is therefore a cerebral trouble pri- 
marily. In these as well as in the cases due to a general hereditary 
agenesis, the cord lesion may be sharply limited to the pyramidal tracts, 
but it is a secondary manifestation dependent upon brain defects. 

In spinal spastic paralysis it is presumed that there is a primary 
degenerative sclerosis, limited solely to the pyramidal, and especially 
to the crossed pyramidal, tracts. Most of the cases of this slow and 
long running disease that come to autopsy, show lesions elsewhere than 
those of these tracts. There is always an open question, therefore, as 
to the priority, importance and inter-relationship of these various 
lesions, in their bearing upon the pathogenesis of the particular dis- 
ease under consideration. It is this that casts a doubt upon the exist- 
ence of the pure type of spastic spinal paraplegia. It is but just to say, 
however, that in a few cases examined by Dejerme and Sottas, Striim- 
pell and others a degenerative sclerosis was found, confined absolutely 
to the pyramidal tracts. Whether this was merely an advanced lesion 
in a more general disease process, and whether, if the patients had lived 
longer, they would have developed other areas of sclerosis as a part of 
the same general disease process, no one can yet affirm or deny. 

Symptoms. — The symptoms of the hereditary and acquired forms 
of the disease are the same, assuming the above limited pathology. In 
most of the so-called hereditary forms the secovdary nature of the 
spinal trouble is intimated in the frequent presence of cerebral symp- 
toms and other indications. 

In the classic type of the disease the only symptom is the spastic 
paralysis with its usual accompaniments of muscular rigidity, rctlc.v 
exaggerations and contractures. This symptom appears gradually, 
passing through an early stage of weakness; then progressing steadily, 
it continues to be the sole manifestation to the end. It appears first and 
advances farther in the legs than in the arms. Often it remains in the 
lower limbs. Sometimes it implicates one leg more than the other. 
The extremity feels tense and stiff at first, as if the tendons were con- 
tracted or were too short. Rapid movements become difficult. Grad- 
ually the gait assumes a characteristic manner. Rigidity is observed 
in all passive as well as active movements. The reflexes now manifest 
a high degree of exaggeration/ The slightest tap on the patella tendon 
evokes a violent jerk. 'Hie cutaneous reflexes are also greatly height- 



HE NEURONIC DISEASES 

FIGURES 83 AND 84. 



423 





FIGURE 83. 

Spastic paraplegia of an adult. Striimpell'j 
medulla. Fig. 84, cfhrical section. Fig. 85, mid 
section. ( After Jak< b. I 



424 



THE NEURONIC DISEASES 



ened. The muscles are undiminished in size and the electrical responses 
remain normal. Gradually a distinct spastic paresis comes on until 
walking is practically impossible, or only possible with short, laborious 
sliding steps on the balls of the toes. The legs incline toward strong 
adduction and the progression becomes "cross-legged." 

With all this serious motor trouble in the legs, and sometimes 
even to a less degree in the arms, there are absolutely no sensory symp- 
toms, no trophic manifestations, no involvement of the sphincters. In 
fine, there is nothing abnormal about the patient but this one manifesta- 
tion, spastic paralysis, though this is. so protean that it represents a 
most profound sort of disability. Late in the disease, even after many 
years, the sphincters sometimes become involved, sensory symptoms 
appear and even ocular troubles supervene. It is a question then 
whether such manifestations do not remove the case at once from the 
classical type of primary spastic paralysis. They certainly would if 
they showed themselves earlier. 

The diagnosis of primary spastic paralysis is always, therefore, a 
provisional one, and at best is always questionable. The disease may 
unmask itself at any time and reveal the symptoms of another trouble, 
such, for instance, as multiple sclerosis, myelitis, amyotrophic lateral 
sclerosis, vertebral tumor or hydrocephalus. 

As a clinical entity the spastic-paretic-symptom-complex may last 
very many years and progress so slowly as to interfere for a long time 
but slightly with the patient's usual avocation. It may even come to a 
complete standstill. 

The mind is never affected. The infantile cases in which epilepsy, 
mental deterioration and other cerebral symptoms occur do not belong 
here. They fall into the group of the cerebral palsies of childhood. 

Diagnosis. — The diagnosis of spastic spinal paralysis is essentially 
the diagnosis of a mere symptom-complex. It is easy in typical cases. 
In atypical cases it must include the larger disease of which the spastic 
paraplegia is but one indication. Elsewhere under the heads of myelitis 
and other cord diseases, and the various cerebral troubles in which 
secondary spastic paraplegia may occur as a residual condition, the 
diagnosis will be touched upon. 

Spastic paraplegia sometimes is witnessed in hysteria. It is rarely, 
however, the only symptom. As a hysterical concomitant it appears 
abruptly and is subject to psychical influences. Care must be exer- 
cised not to mistake a spastic paraplegia for the hysteroid manifesta- 
tions that may occur sometimes in incipient disseminated sclerosis. 
There is a treacherous similarity at times between multiple sclerosis 
and hysteria. Spastic paraplegia, organic in the one case, psychic in 
the other, is not an uncommon phenomenon in both. Further details 
in regard to the differential diagnosis may be gathered from the discus- 
sion elsewhere of these two affections. 

Treatment. — The treatment of the disease is an ungrateful task. 
Care as to the nutrition, avoidance of exhaustion, massage and gym- 
nastic exercises constitute about all that we can do. Contractures and 
deformities are to be managed on general orthopaedic principles. The 
younger the patient, so much the more promising are the* results to 



THE NEURONIC DISEASES 425 

be expected from these general measures. These patients often enjoy 
excellent general health and live many years. They must be taught 
to exercise patience and to make the best of a very chronic state of 
invalidism. Medicines are of no avail, and as there is little real suf- 
fering beyond the inconvenience of locomotion, symptomatic treatment 
is rarely called for. 

SPASTIC PARAPLEGIA OF CHILDHOOD. LITTLE'S DIS- 
EASE. 

The infantile form of spastic paraplegia, as usually described in 
the books, is a double hemiplegia. It is a question whether such a name 
as paraplegia cerebralis spastica should not be dropped entirely. A 
paraplegia has come to mean technically a spinal cord trouble, there- 
fore to speak of a cerebral paraplegia is not only misleading, but is a 
contradiction of terms. Xeither symptomatica! ly nor pathologically are 
these diplegias of childhood spinal cord affections. Including Little's 
disease, they are, so far as the spinal changes are concerned, merely 
secondary degenerations of cortical origin. They bear a symptomatic 
resemblance, to be sure, to the primary spastic paraplegia of adults. 
The reflexes are highly exaggerated, but the spasmodic jerk is not so 
vigorous as it is in the adult disease. Foot clonus may sometimes, but 
very rarely, be obtained. 

In some cases the muscular power is not much diminished, but 
walking is quite difficult on account of the contvacturcd condition of the 
calf muscles, the strong adduction of the legs and the tendency in the 
gait to the "crossed-legged progression." There is no true muscular 
atrophy, though the legs do not develop and grow as they should. 
Some of the cases may resemble Charcot's amyotrophic lateral scler 
in its early appearance, and then exhibit a certain amount of true mus- 
cular atrophy. Amyotrophic lateral sclerosis is an adult disease, how- 
ever, rarely, if ever, occurring before ten years of age ; it involves the 
arms most extensively; and is distinguishable from infantile spastic 
paraplegia by other signs. It was the more or less limitation of the 
paralysis to the lower limbs, and the absence of all cranial symptoms, 
that led the earlier authorities to attribute the symptoms and the entire 
disease to the spinal cord. In the arms, however, there may be observed 
choreic phenomena and usually a considerable degree of athetosis. 
These arm symptoms are slight in the cases thai may fairl\ be denom- 
inated "spastic paraplegia." 

The entire question as to the classification of these cases depends 
upon the primary or secondary nature of the spinal cord changes. If 
the cord changes are primary, a condition which would be ver\ 
ceptional and in my own opinion extremely doubtful, there is no need 
of creating a new disease i ul of what would then be an ordinar) pri- 
mary spastic paraplegia, merely on account of the age of the victim. 
Granting that Van Gehuchten, Souques, Raymond and Erb arc justi- 
fied in their belief that a primary infantile spastic paraph cord 
origin does exist, and that, as Dejerine has found, there is evidence of 
cervical degeneration, with secondary degeneration of the pyramidal 



426 THE NEURONIC DISEASES 

tracts, occurring during fetal life, the point is still more strongly 
emphasized that there is no need of writing a new section, and describ- 
ing these infantile cases apart from the general description of the ordi- 
nary or adult form of the trouble. On the other hand, if the cord 
changes in these cases are secondary to the cortical lesion, as shown by 
the frequent epilepsy, cranial nerve palsies and psychical disorders in 
addition to the pathological findings, there is again no need of elevat- 
ing the condition into one of a special and unique form of disease. 
It is then but a particular manifestation of double hemiplegia, a diple- 
gia, and falls naturally into the discussion of brain diseases. 

SECONDARY SPASTIC PARALYSES. 

The many hemiplegic, quadriplegic, diplegic and paraplegic condi- 
tions that follow intracranial and intraspinal lesions arising in the non- 
neuronic tissues are not strictly to be considered here, for the degenera- 
tion is of the secondary or rather Waller ian type, and the primary 
disease which is really of extra-neuronic origin is the prominent feature. 
Thus- inflammatory conditions, neoplasms, compressions, vascular 
lesions of all sorts are commonly followed by degeneration of the 
descending type in the neurones caught in the damaging processes. 
This degeneration Is, as it were, a sort of a sequel of the disease. It 
has its own prognosis and treatment, but they are not the prognosis and 
treatment of the disease in which they occur. 

These secondary neuronic degenerations will be considered in 
detail elsewhere in connection with the diseases out of which they 
spring. 

Sometimes it is very difficult to distinguish the primary spastic 
paralyses from the secondary. A sharp distinction between the two. 
thus made in the classifications, will, it seems to me, help toward the 
making of the differentiation in the diagnosis. At all events it will 
emphasize the differences between the prognosis and the treatment of 
the two sets of diseases. 

Primary neuronic degenerations are apparently diseases sni generis 
and are hopeless in their outlook and unsatisfactory in their treat- 
ment. 

Secondary neuronic degenerations are the sequels of diseases 
which are hopeful and satisfactory to treat in spite of the hopelessness 
of the secondary results. 

C DISEASES OF THE LOWER .MOTOR SEGMENT. 

The degenerations involving the lower motor neurones are in- 
numerable, but they are both primary and secondary in origin. The 
former we know less .about than we do of the latter. All severe lesions 
that damage the cranial nuclei, the anterior horns of the cord, and the 
peripheral nerves may cause the neurones in their vicinity to undergo 
a progressive degeneration. In this way the polioencephalitic, polio- 
myelitic and peripheral neuritic diseases are all more or less followed 
by degenerative paralysis. This paralysis, however, is virtually a 



THE NEURONIC DISEASES 427 

sort of a sequel of the disease. It may be very prominent and demand 
its own consideration, as in acute anterior poliomyelitis, for instance. 
but it is not the disease itself. Its prognosis should not be confounded 
for a moment with the prognosis of the affection out of which it has 
sprung. It, of course, like all neuronic degenerations, is systemic in 
its distribution. I see no reason, however, for employing it as a basis 
for the classification of the disease. It is a false classification, it seem- 
to me, that includes among the system diseases chronic poliomyelitis 
and not cerebral embolism. It would be a still more unreliable classifi- 
cation that would consider either as a systemic neuronic disease. 
Poliomyelitis is an inflammation with certain secondary neuronic de- 
teriorations, even as cerebral embolism is a vascular trouble with like 
secondary neuronic wasting. Of these secondary atrophies, the one 
is below in the spinal anterior cornual neurones, the other is above in 
the cerebral cortical neurones. All such degenerations should be 
considered merely as one of the results of the primary disease and 
should in no way be made the basis of their classification. 

It is frankly admitted that there are many degenerative conditions 
in the lower motor segment that we cannot yet affirm positively to be 
either primary or secondary. Most of them are undoubtedly secondary. 
The few that seem to be primary will be briefly referred to here. 

OPHTHALMOPLEGIA. 

The nuclei of the motor nerves of the eye, the third, the fourth and 
the sixth, lying along the aqueduct of Sylvius are the homologues of 
the anterior horns of the cord. They contain the cell-bodies of the 
neurones that innervate the ocular muscles, just as the horns contain 
the cell-bodies of the neurones that pass out of the anterior roots and 
innervate the muscles of the body. These nuclei undergo the same 
sort of degenerative and inflammatory processes that the horns do 
and, like the latter, they can give rise to an atrophic paralysis that may 
pick out individual ocular muscles. This is termed Ophthalmoplegia, 
which for clinical convenience is divided into internal ophthalmoplegia, 
when the internal ciliary muscles and iris are involved, and external 
ophthalmoplegia when the external recti, the oblique and palpepral 
muscles are implicated. 

A bilateral external ophthalmoplegia, with intact ciliary, iris and 
lid muscles, is pathognomonic of a nuclear lesion, for no peripheral 
nerve trouble could hardly present such ;< clinical picture. The nuclear 
disease max be aeute and vascular. It would be described then ;is .1 
particular form of polioencephalitis, often as ;i part of Wernicke's type 
of acute hemorrhagic polioencephalitis superior, mentioned elsewl 
under inflammations of the brain. 

Infection and intoxication are die chief causes of acute ophthal- 
moplegia. This form of the disease max or ma) noi have a discover 
able pathological change as its anatomical basis, according to the 
virulence of the toxin and the duration of its action. 

The prognosis is noi very favorable in tin alcoh 



428 THE NEURONIC DISEASES 

recoveries often occur in the influenza and other toxic cases. This,, 
of course, is a secondary degenerative process. 

Chronic ophthalmoplegia is a slow, progressive degenerative dis- 
ease which aligns itself easily with the progressive muscular atrophies. 
In fact, it is not infrequently the precursor of various degenerative 
system diseases, such as tabes, progressive bulbar paralysis, progres- 
sive muscular atrophy, etc. It occurs also as a part of the combined 
diseases of the cord, of multiple sclerosis and of progressive paralysis. 
It is associated with psychic disorders. It has been seen as a con- 
genital trouble, as a part of an inherited familial degeneration. Op- 
penheim is convinced that syphilis can provoke the degenerative process. 
A slow hemorrhagic cause may be possible. 

Pathologically the disease is a primary degeneration of the neu- 
rones of the nuclei of the ocular motor nerves. 

Symptoms. — These come on gradually and often are not remarked 
until the disease is well advanced. The vision of the eyes individually 
is not affected, and as the trouble is so slow and insidious, when the 
lines of vision are disarranged on account of the palsy, the patient 
becomes habituated to a monocular vision. Gradually the loss in the 
mobility of the eyeball is noticed. There is a slight strabismus, more 
frequently divergent. Examination with the moving finger reveals 
the limited excursion of the eyeball in attempting to follow it. The 
eyelids droop and what is termed the "Hutchinson face" is presented. 
Sometimes amblyopia is complained of. The pupil as a rule is intact 
and reacts well to both accommodation and light. 

Prognosis. — The disease is a very chronic one and the prognosis- 
is unfavorable. Sometimes it becomes stationary. Optic atrophy often 
combines with it, especially when it is a part of some general systemic 
degenerative trouble. 

Treatment. — For the acute cases the treatment is along general 
antiphlogistic lines and includes purgation, baths to provoke sweating, 
ice bags and temporal bloodletting. A history of syphilis points out the 
proper therapy to resort to, while in all cases the causative factor, if 
such can be found, must receive the brunt of the attack. Galvanism has 
been recommended ; upon what ground it is hard to conceive. Reme- 
dies that have been used and are still recommended, but are generally 
ineffectual, are strychnia, arsenic, potassium iodide, phosphorus and 
general tonics. 

Primary Degeneration of the Other Cranial Nerves is exceedingiv 
rare as an isolated process. A few congenital bilateral facial palsies 
have been seen, and unilateral nuclear disease of the hypoglossal has 
been reported. Such cases are always unique and we have no knowl- 
edge of their true anatomical basis. Most of the primary degenera- 
tions of these nerves belong to the bulbar palsies and will be described 
under that head for the sake of convenience, or to the bulbar manifesta- 
tions merely of other more general troubles, such as progressive mus- 
cular atrophy, general intoxications and specific infections, where they 
will receive their appropriate consideration. 

( )f primary degeneration of the spinal motor nerves we know- 
nothing, if indeed it ever occurs. Some forms of toxic peripheral 



THE NEURONIC DISEASES 429 

neuritis may be primarily degenerative and for aught we know be 
limited to the motor neurones. It is doubtful, however, as in these 
cases inflammatory and sensory symptoms are often present. 

MYASTHENIA GRAMS. 

This is believed to be a bulbar disease, as is indicated in the names 
asthenic bulbar paralysis and bulbar paralysis without discoverable 
anatomical lesion; but its functional neuronic character depending, as 
most authorities think, upon a dynamic disturbance in the lower motor 
neurones, it may for the present be classified here. A number of cases 
of the disease have now been reported. I can add to them one that I 
was recently consulted about, which has since died after presenting for 
several months a very typical clinical picture, and which seemed to 
follow an aborted attack of scarlet fever. 

Etiology. — Middle-aged and young persons are usually selected 
as victims. Chlorosis and a hereditary taint were noted in one case 
by Oppenheim and Bruns. Toxaemia was strongly suggested in my 
case. The man was a teacher in a college where there had been a 
slight epidemic of scarlet fever. He had a faint, evanescent rash and 
signs of an aborted attack. Later on he assisted in the formaldehyde 
fumigations and shortly after this showed the first signs of weakness. 

Pathology and Pathogenesis. — There is nothing known of this, 
as no anatomical lesions have been found. 

Symptoms. — As the name myasthenia gravis indicates, the prom- 
inent symptom, of this disease is the profound muscular weakness, 
with remarkable remissions in the weakness. The disease lasts often 
many months and in that time the patient has spells of such weakness 
that he will keep his bed ; and yet he will recover so much that hopes 
will be awakened that he has fully gotten well again. The hopes are 
soon seen to be fallacious, for on comes the weakness, almost paralysis, 
again. And thus he goes, up a few weeks, then down again, the 
weakness disappearing from this group of muscles, to reappear later 
on in another group. The muscles supplied from the medulla are so 
frequently affected, and so often are the cause of the patient's death h\ 
asphyxia, that the name asthenic bulbar paralysis has been given to the 
■disease. Other muscles of the body, however, are usually implicated. 
Ptosis is particularly common. It was almost the first symptom in 
my case. The muscles of the trunk and extremities are affected. All 
acts and all movements are restricted. The patient feels as though he 
could walk as well as any one, but the moment he gets up he begins 
to weaken and he is chagrined to find that the feeblest efforts, the 
shortest walks, completely exhaust him. Talking becomes a tremen- 
dous task. Sometimes he can't masticate and swallow Ins food. 

A remittent, chronic, progressive glosso-labio-laryngeal paralysis, 
with weakness and palsy in other parts of the body, constitute tin- 
motor side of this singular malady. Sometimes the bladder and rectal 
functions are also implicated. The muscles are norma] m size and do 
not reveal any abnormal electrical reactions. Noticeable variation of 
the weakness, from a moribund state altnosl to complete health, and 



430 THE NEURONIC DISEASES 

then back again to a moribund state, and marked, almost dangerous 
exhaustion are the striking features in the course of the disease. There 
are no sensory symptoms and the mind continues clear. 

Diagnosis. — This must be made from the character of the weak- 
ness and palsy, the remissions during the progress of the disease, the 
absence of organic muscular changes, the absence of sensory and men- 
tal symptoms and the probable etiology. Hysteria can be differentiated 
by the presence of sensory and mental phenomena. Poliomyelitis, or 
rather polioencephalomyelitis and muscular dystrophy, do not remit as 
this disease does, and they exhibit organic muscular signs such as the 
muscular atrophy and electrical changes. There are some things about 
this disease that lead one to compare it with Landry's syndrome. The 
latter has even appeared first with the bulbar complexus of symptoms. 

Prognosis. — The malady is almost universally fatal, though a few 
cases have gotten well. The trouble appears acutely or insidiously, 
but it generally runs a remittent, chronic course. It is a dangerous dis- 
ease, as one can never tell when death may come. The latter usually 
results from asphyxia or exhaustion. 

Treatment. — Rest and quietude in bed is about the best we can 
do. There is a strong temptation to use electricity, but it is a danger- 
ous procedure. Moreover, it could hardly be expected to do any good, 
from the nature of the trouble. When the patient cannot swallow a 
stomach tube may be used, but it involves a great risk. Oppenheim 
lost a case during the manipulation. If there is the slightest degree of 
spasm from the introduction of the tube, the treatment had better be 
desisted. Simple tonics and a mild diaphoretic treatment might prove 
available, for it is probable that the basis of the trouble is an intoxica- 
tion or infection of some sort. 

OCCUPATION MUSCULAR ATROPHY. CRAFT PALSY. 
PROFESSIONAL PALSIES. 

This is a borderline degeneration which in some cases is undoubt- 
edly primary, while in others it is secondary and is associated with a 
neuritis. 

The constant use of certain nerves and muscles in one monotonous 
manoeuvre, demanded by certain occupations, sometimes leads the lat- 
ter to undergo an atrophic paralysis. Oppenheim mentions a weaver 
who had to extend his forearm about twenty thousand times a day 
and who thereupon suffefed from an atrophic paralysis in the right 
triceps muscle. In this way locksmiths, paper-glazers, blacksmiths, 
cabinet-makers, gold-polishers, oarsmen, cigar rollers, drummers have 
been afflicted. Of course, the trouble is mostly seen in the upper ex- 
tremity. Potato-pickers, seed-sowers and those who kneel a great deal 
may have the trouble in their lower limbs. Ballet dancers have thus 
had their calf muscles affected. 

These cises must not be identified with the occupation neuroses, 
which are due to a disturbance in the central eoodinating apparatus, 
rhese cases are to be attributed to over-exertion, pressure, even lacera- 
tion of the nerves in which run the lower motor neurones. There is an 



THE NEURONIC DISEASES 43 1 

atrophic condition started in this way in these neurones which in most 
instances is quickly recovered from if the member is placed at rest. 
This wasting, however, has in a number of instances, in spite of the 
use of all preventive measures, gone on to the production of a pro- 
gressive muscular atrophy. General intoxication* with alcohol, lead, 
infection from influenza, general marasmus and a previous history of 
acute anterior poliomyelitis seem to favor this unfortunate turn to the 
paralysis. In some cases there have been slight paresthesia?, and pains 
and other sensory manifestations that have suggested an interstitial 
neuritis. In still other cases the trouble is probably due entirely to the 
muscle and not at all to the nerve, in this way intimating what we have 
long been suspecting — namely that there is no sharp line of division to 
be drawn between the atrophies and the dystrophies. 

Most of these craft palsies get well under favoring conditions, for 
the atrophy, whether primary or secondary, does not go on to the 
stage of incurability. \\ 'hen, however, it passes into the progressive 
form, the prognosis is hopeless. 

The treatment consists of rest, the careful use of galvanism, 
hypodermics of strychnia and a general tonic and health-producing 
regimen. 

ACUTE ASCENDING PARALYSIS. LANDRY'S PARALYSIS. 

Landry described in 1859 a form of motor paralysis in which there 
were no sensory symptoms, no muscular wasting, no electrical reac- 
tions, no bedsores or other trophic manifestations, no involvement of 
the bladder or rectal functions. The paralysis was flaccid in character, 
ascended rapidly up the body and usually terminated in death in a few 
days or a week, from respiratory involvement and other bulbar symp- 
toms. There were no post-mortem findings and so Landry. Westphal 
and others attributed the trouble to some form of acute poisoning. 
Later on when it was found that some cases of acute ascending paralysis 
exhibited slight sensory symptoms, and a mild degree of muscular 
atrophy, with a loss of the deep reflexes and with certain electrical 
changes, it was believed that Landry had described merely a form of 
multiple neuritis. Comparisons were drawn between it and the symp- 
toms produced often by such forms of intoxication as alcohol, curare, 
lead and the infections. It soon became clear that Landry had not 
described a new disease, but a symptom-complex often observed in the 
early stage of virulent forms of intoxication. In one sense, therefore, 
the term acute ascending paralysis covers more than the term Landry's 
paralysis, while the latter, in its original, narrow definition, is but one 
manifestation of a profound intoxication of which there may be other 
and later manifestations according to the susceptibility of the nervous 
system involved, the virulence of the poison or the duration ^i its 
action. 

Etiology. — Some form of profound intoxication of bacterial origin 
seems to be at the bottom of Landry's paralysis. Neither the particu- 
lar toxin nor the micro-organism has ben isolated yet. The disease 
seems most frequently to follow, or to be associated with, the infectious 



432 THE NEURONIC DISEASES 

fevers, notably typhus, typhoid, pneumonia, variola, pleurisy, diphtheria, 
anthrax, influenza, pertussis, gonorrhoea (?), syphilis, septicaemia and 
rabies — a most suggestive list ! Other contributing causes have been 
named by various writers — namely, exposure to cold, the puerperium, 
suppressed menstruation, coitus in the standing posture and mental 
excitement. It is probable that these were mere coincident circum- 
stances, or at most assisted only in provoking the intoxication or auto- 
intoxication underlying the disease. Men are more subject to the 
trouble than women are, the proportion being put by some as high as 
twelve to four. The middle period of life, twenty to forty, is when 
the disease occurs most frequently. It will be noted, as Gowers well 
remarks, that the remote etiology of acute ascending paralysis re- 
sembles in general that of acute myelitis. 

Pathology and Pathogenesis. — According to the earlier obser- 
vations of Landry, Westphal and others, a remarkable peculiarity of 
this disease was the absence of all post-mortem findings. Landry 
therefore concluded that the trouble was due to some form of poison- 
ing, a view which Westphal was the first to establish upon a scientific 
basis. Even to-day, with our more improved methods of investiga- 
tion, there are cases in which no pathological changes can be discovered 
at the autopsy. Such cases, however, are becoming less and less fre- 
quent every year. In other words, the greater number of the cases 
nowadays reveal changes of an inflammatory and degenerative type 
in the nervous system, and more or less the appearances of a septic 
condition in the other organs. These changes are indefinite, varied 
and scattered, just as we would expect in a general toxaemia. Dissem- 
inated foci of inflammation with exudation and capillary hemorrhages, 
have been observed in the medulla, particularly the pyramidal tracts. 
Similar changes and other myelitic processes have been found in the 
spinal cord. Anterolateral tracts have been affected. In some cases 
there were findings of a typical poliomyelitis, but of a slight degree. 
Oppenheim says that in one case a degeneration of the anterior roots 
was the only alteration ; in another a small myelitic focus in addition 
to a peripheral neuritis. The lesions of the peripheral nerves have been 
observed frequently enough to incline some authors to regard the dis- 
ease as a peripheral neuritis. Outside of the nervous system the 
changes most commonly found included enlargement of the spleen, 
pleuritic adhesions, hemorrhagic foci in the lungs and bowels, inflam- 
mation of the lymph glands, especially in the intestines and mesentery, 
and albuminuria. 

All of this indicates plainly the toxic origin of the trouble. The 
bacterial source of the toxin is based upon strong evidence, though as 
yet no specific micro-organism has been isolated. The researches of 
Baumgarten, Eisenlohr, Centanni, Curschmann, Remmlinger, Oettinger 
and Marinesco, Marie and Marinesco, Bailey and Ewing, Seitz, Thoi- 
not and Maselli, and Buzzard are almost conclusive. By these investi- 
gators various bacteria have been found in the nervous tissues of pa- 
tients dying of acute ascending paralysis. By some of them the germs 
have been cultivated, injected into animals and thus a set of symptoms 
provoked identical in all respects with those of the disease in man. 



THE NEURONIC DISEASES 433 

In the modern sense, Landry's paralysis cannot be regarded as a 
distinct pathologico-anatomical entity, in spite of the fact that clinically 
it affords a fairly definite symptom-complex. It is the expression of 
an intoxication of bacterial origin, some cases running their course so 
rapidly as to leave no discoverable lesions, while others of a slower or 
less virulent type exhibit various, diffuse, infectious lesions. Why this 
intoxication should seem to select the peripheral motor neurone in 
most cases whereon to expend its force primarily it is hard to say, 
but that it is not limited solely in all cases to that neurone is shown 
by the sensory and other symptoms. This may be explained when we 
know more about the relative susceptibilities of the different parts of 
the nervous system, or when, perchance, we discover, if we ever do, a 
specific germ as the cause of the intoxication. 

The diffuse character of this poison and the irregularly scattered 
location of the lesions which it provokes may well cause Landry's 
paralysis to closely simulate a diffuse myelitis, an anterior poliomyelitis 
or a multiple neuritis. They are not the same, however, as will be 
pointed out under the head of diagnosis. 

The cases that succumb rapidly are apparently primary, profound 
intoxications of the neurones. For this reason I place the disease pro- 
visionally here. "When it is shown to be always a pure inflammatory 
trouble, it will then be removed from the class of neuronic affections of 
primary origin. 

Symptoms. — Usually there are premonitory symptoms, such as 
a feeling of general malaise, numbness of the extremities, slight pains 
in the back and elsewhere, weakness of the legs with tingling and 
other symptoms not unlike those found in neurasthenia. These prodro- 
mata may last several days and gradually pass into the typical symp- 
tomatology. Many cases, however, begin abruptly with a decided 
weakness in one or both legs, which in a few hours become completely 
paralyzed. The paralysis then rapidly travels up the body, involving 
successively the trunk, the arms and finally the muscles of respiration 
and deglutition. The patient cannot sit up on account of the paralysis 
of the back muscles. Coughing, sneezing, defecation and urination are 
all difficult when the abdominal muscles are involved. Swallowing and 
breathing become embarrassed and in the end impossible. 

In a case reported by Westphal the medulla oblongata alone was 
implicated, the disease beginning and terminating with bulbar symp- 
toms. 

The paralysis is not always paraplegic in its distribution or ascend- 
ing in its course. Sometimes it skips about from the arm to the leg 
or vice versa. Fagge declares that the great naturalist Cuvier died of 
a rapidly descending Landry's paralysis. 

As a rule the deep reflexes arc lost, but the muscles are not atro- 
phied and the electrical irritability remains normal. There is no f 
except in a very few cases, in which there has been observed a slight 
temporary elevation of the temperature. The sensations arc unaffected. 
Trophic abnormalities are absent. The rectal and bladder functi 
are undisturbed. Finally the speech grows heavy and indistinct, swal- 
lowing becomes impossible, respiration grows rapid or assumes the 



434 THE NEURONIC DISEASES 

Cheyne-Stokes characteristics, and death ensues in a few days, usually 
less than a week, under asphyxia. The mind remains clear to the last. 

Such is the acute ascending paralysis described by Landry. 

Even to-day many authors limit the name Landry's paralysis to 
the above described symptom-complex. The more modern conception 
of the disease, however, presents a broader clinical picture. For ex- 
ample, with the paralysis in some cases are associated a moderate de- 
gree of muscular atrophy, sensory and trophic symptoms, and involve- 
ment of the bladder and rectal sphincters. Moreover, the distribution 
of the paralysis is less regular and the progress of it less rapid than as 
Landry originally described it. And instead of the disease being so 
universally fatal, not a few cases have gotten entirely well after several 
weeks' duration. Many of these later cases bear a close resemblance 
to acute ascending meningo-myelitis, disease of the spinal roots and 
multiple neuritis. 

The sensory symptoms when present are very variable. At first 
there is numbness, formication and other paraesthetic manifestations. 
A slight loss of sensation is common ; a complete anaesthesia is rare. 
Hyperesthesia has been observed. Analgesia is sometimes present, 
and even the muscular sense has been found to be altered. Thus every 
variety of sensory disturbance may be expected. These symptoms are 
doubtless due to a secondary involvement of the sensory apparatus, as 
Landry's paralysis would seem to be primarily a disease of the motor 
apparatus. 

As a rule the slight diminution that occurs in the muscle-masses, 
when the patient lives long enough, is not the same as the typical 
atrophy that is observed in acute anterior poliomyelitis. Even after 
many weeks there is still no atrophy nor any alterations of the electrical 
reaction. Exceptionally, however, there is distinct,, typical muscular 
atrophy and a characteristic reaction of degeneration. Remak errone- 
ously thought that this absence of muscular atrophy and normal elec- 
trical irritability were pathognomic of Landry's disease. ' 

In exceptional cases the bladder and rectal functions have been 
affected. According to Oppenheim, even complete paralysis of the 
sphincters has been observed. In many of the cases there may be for a 
short time retention of the urine, but as this soon passes off, there is 
seldom need for the employment of the catheter. 

The cranial nerves, other than those spoken of in connection with 
the respiration and deglutition, escape. In rare cases the facial and 
motor-oculi have been implicated. 

As a rule there is no fever, no delirium, no clouding of the mental 
faculties. In a few cases there have been recorded high fever, signs 
of general septic infection and more or less obliteration of conscious- 
ness. It may be well questioned whether such manifestations should 
be included under the head of acute ascending paralysis rather than 
that of a general septic state of which the paralysis is a concomitant 
symptom. In these cases hyperidrosis has often been described. 

Diagnosis. — Multiple neuritis of infectious origin has been identi- 
fied with Landry's disease (Ross, Dejerine and Goetz, Nauwerck and 
Barth, Putnam, Klumpke. Krewer, Pitres and Vaillard, Mobius, Kiril- 



THE NEURONIC DISEASES 435 

zew and Mamurowsky, Spiller and others), and yet. as Oppenheim 
well says, it is not proper to regard them as perfectly identical. Lan- 
dry's paralysis of the pure type differs from multiple neuritis in the 
absence of distinct pain and other sensory disturbances, in the non- 
atrophic condition of the muscles and the preservation of the normal 
electrical irritability. Meningeal hemorrhage may be distinguished by 
the pain in the back and the spasm. Acute anterior poliomyelitis does 
not exhibit the peculiarly rapid, ascending, mere or less paraplegic 
form of paralysis characteristic of Landry's symptom-complex. The 
former is notable for the distribution of the paralysis in particular 
muscles or groups of muscles, which quickly undergo atrophy and 
manifest well-known abnormal electrical reactions. Aente myelitis or 
menin go-myelitis of the ascending type is to be differentiated by the 
presence of fever, sensory troubles, bedsores and other trophic mani- 
festations, and vesical and rectal phenomena. 

After all, however, it must be admitted that there are some cases 
of Landry's syndrome that cannot clinically be distinguished from any 
one of these, especially from multiple neuritis and acute anterior 
poliomyelitis. And this is not to be wondered at when one recalls the 
nature and pathogenesis of Landry's group of phenomena. The same 
observation will explain the futility of arbitrarily dividing the disease 
into three distinct types, the bulbar, spinal and peripheral ; or of mak- 
ing such a separate variety as the descending form, in contradistinction 
to the ascending. 

Prognosis. — The course of the disease is variable and the prog- 
nosis always grave. It is not always fatal, however, as it was at one 
time considered. Sometimes death takes place in a tew hours, or in 
two or three days, and sometimes it is postponed for three or four 
weeks. The rapidity, duration or completeness of the paralysis does 
not seem in any way to measure the gravity of the disease. The char- 
acter of the bulbar symptoms and the degree of involvement of the 
functions of respiration, deglutition, etc., are the guides to be closely 
watched in forming a prognosis. Steadily progressing cases, even 
though slow, are unfavorable. Cases have recovered, a fact which 
justifies a favorable outlook, if there is the slightest retrocession in the 
progress of the malady. The fatal cases usually terminate inside of 
a week. 

Treatment. — Recognizing the toxic origin of Landry's paralysis, 
it is obvious that the ideal treatment would be the use of an antitoxine. 
There is none known, however, and so we must still resort to all m 
ures calculated to support the patient's vitality and to eliminate the 
poison as rapidly as possible. Unfortunately the rapidity of the dis- 

too often forestalls all such commendable efforts. Nevertheli 
it is wise to resort to mild stimulation with alcohol, ammonia and other 
diffusible stimulants, to give an abundance of easily digested and easily 
assimilated nourishment, and to increi Far as possible, the func- 

tions of the emunctory organ-. Warm baths and hot wet packs stimu- 
late the skin into renewed activity. Counter-irritation over tin- spine, 
and especially over the region of the kidneys, should be resorted to. 
The action of the kidneys should lie favored bv tin- n<e >^\ diuretics with 



436 THE NEURONIC DISEASES 

the drinking of an abundance of wafer. Free catharsis is advisable 
with calomel or elaterium, followed by salines. When swallowing be- 
comes difficult nourishment and medicines should be administered by 
the rectal or nasal tube. 

As for medicines, there are none known upon which we can rely 
with certainty. In one case following exposure to wet and. cold, and 
almost at the point of death, ergotin in two-grain doses every hour was 
followed by a speedy recovery. Salicylate and benzoate of sodium have 
been recommended. Iodide of potassium and mercury have had their 
advocates, irrespective of the possible cause of syphilis in some cases. 
Belladonna has been tried with doubtful results. As for the use of 
strychnia, one would feel some hesitancy about employing so vigorous 
a spinal stimulant in a disease in which there are inflammatory and 
degenerative changes going on. 

In a word, the nature of the disease, and the results so far ob- 
tained, indicate a revulsive line of treatment, w T ith the use of anti- 
phlogistic and diaphoretic measures. Perhaps some day blood-serum 
therapy will make all such crude measures unnecessary. 

PERIODICAL PARALYSIS. 

This is perhaps the place to refer briefly to a remarkable form of 
paralysis that comes and goes periodicallv. 'The phenomenon has been 
seen particularly in connection with the movements of the"eye and of the 
extremities. 

Periodical Paralysis of the Extremities. With or without an an- 
aesthesia an intermittent paraplegia of the arms and legs occurs, com- 
ing on with great regularity, without apparent cause, when the pa- 
tient is in the full flush of health, awake or asleep. Weakness of the 
limbs, weariness and drowsiness, and occasionally paraesthesiae precede 
it. Twenty-four hours usually sees the paralysis complete. The arms, 
the legs, the neck and occasionally the tongue and pharynx are in- 
volved. The cranial nerves are unaffected as a rule. There is no fever, 
but the temperature is often subnormal and the pulse slow. 

The heredity in the disease is quite marked, so much so that it 
assumes the form of a "family" disease. Goldflam, for instance, saw a 
family with twelve afflicted members, the heredity being through the 
mother. Taylor saw eleven cases in five generations of a family. This 
with other features of these periodical paralyses makes one think strong- 
ly of a hysterical affection, but there is a remarkable stumbling block in 
the way of regarding it as hysterical. Functional as the disease 
appears to be, there is a reduction, sometimes abolition, of the reflexes ; 
and stranger yet than all, a reduction or complete abolition of faradic 
excitability of both the muscles and the nerves. This looks very much 
like a toxic neurosis or temporary infection involving especially the 
lower motor neurones. Nothing but toxaemia would produce such a 
localized, short-lived paralysis. It is not impossible that the toxin, 
whatever it is, may be periodically evolved in the patient's own body, as 
the result of his inherited neurotic defect. This is the only sort of a 
hypothesis that would harmonize all the features of these strange par- 



THE NEURONIC DISEASES 437 

alyses. The evolution of the toxin results periodically from an inher- 
ited neurosis. This expends itself upon the lower motor neurones and 
we have the incipiency of an organic neuronic disease, which, however, 
does not last long enough to provoke permanent changes. 

COMBINED DISEASES OF THE AFFERENT AXD EFFER- 
ENT SYSTEMS. 

It is well known that degeneration and sclerosis in the lateral col- 
umns of the cord occur late in a few cases of locomotor ataxia. This 
is looked upon as a mere complication or sequel and not as an integral 
part of the disease. There are a number of diseases, however, in which 
the hardening of the lateral and posterior columns proceed simultane- 
ously, seem to be dependent upon the same causative influence, and 
exhibit a more or less uniform clinical picture. Heredity plays a sig- 
nificant role as a predisposing cause, while infection and nutritive dis- 
turbances a're prominent among the exciting causes. The cord changes 
observed in pernicious anaemia afford a good illustration of the domi- 
nance of an exciting cause, while Friedreich's ataxia shows well the 
power of a hereditary cause. 

When the disease occurs in childhood, as it does in most of the 
hereditary types, the undeveloped condition of the nervous system nat- 
urally causes a modification in the clinical picture different from that 
which it would have in an adult after the nervous apparatus has ac- 
quired its full growth and has long been subjected to disciplined and 
fixed habits. 

Again, a variation in the clinical exhibition would be wrought, as 
Westphal long ago pointed out, by the rehtive intensity and extent of 
the lesion in the lateral or the posterior columns. If the disease process 
in the posterior columns is in advance of that in the lateral columns, the 
symptoms bear a resemblance in some respects to those of tabes. If 
the disease is more pronounced in the lateral than in the posterior 
columns, the clinical portraiture simulates somewhat spastic paraplegia. 

Clinically, therefore, we find in these combined scleroses two 
prominent features that justify their consideration as distinct and inde- 
pendent affections. The fir^t is the uniformity of the clinical mani- 
festations due to the combined posterior and lateral lesion. The other 
is the particular modification of symptoms evoked by the age of the 
patient and the relative prominence of the lesion in one or the other 
location. Unless these facts are kept well in mind there will be an un- 
necessary refinement of classification and the elevation of mere symp- 
tom groups into distinct and separate diseas 

From what has alread) been said, it is obvious that the combined 
sclerosis of the two columns of the cord, so different in their genera] 
functions as are the lateral and posterior columns, must necessarily pro- 
voke some marked differences between tin- clinical manifestations of 
different cases. 

Theoretically and pathologically there may be no good reason for 
separating from one another the spinal sclerosis of pernicious anaemia, 
ataxic paraplegia, hereditary ataxic paraplegia, Friedreich's disease any 



438 



THE NEURONIC DISEASES 

FIGURES 87, 88 AND 




The combined scleroses or system diseases. Fig. 87, cervical section. Fig. 88, 

dorsal section. Fig. 89, lumbar section (After Jakob.) 



THE NEURONIC DISEASES 439 

more than there is for separating the hemiplegias, diplegias and con- 
genital spastic "paraplegias" among the cerebral palsies of childhood. 
Practically, however, it is advantageous to make the distinction, not 
to emphasize them as distinct diseases, but to point out the individual 
etiology and minor symptomatology in each particular class. 

The highest aim of science is to generalize and not to individual- 
ize. The reduction of all exceptions and their inclusion under a general 
law, as rapidly as knowledge m regard to them will warrant, should 
ever be the purpose of scientific endeavor. Unfortunately in this re- 
spect art and science are often in gentle conflict, and as a result we 
make for practical convenience distinctions and classifications where 
scientifically there are no broad lines of difference. 

For practical purposes then we will do well to carry about in our 
memory the following types of the combined scleroses enumerated by 
Dana: 

i. Combined scleroses of profoundly anaemic and toxic states 
(Putnam's type). 

2. Hereditary spinal ataxia (Friedreich's ataxia and hereditary 
ataxic paraplegia). 

3. Combined scleroses complicating general paresis. 

4. Accidental forms (Gowers', ataxic paraplegia). 

Myelitis, meningomyelitis, posterior leptomeningitis of syphilitic 
and other infectious origin with secondary degeneration in particular 
tracts, will explain a large number of cases reported to belong to one or 
other of these classes. The anaemic and toxic scleroses are clearly not 
distinct disease entities and in many cases they are merely diffuse condi- 
tions such as one observes in all forms of general constitutional poison- 
ing. In pellagra, in ergotism, in leukemia and in carcinoma a combined 
sclerosis of the cord has been observed. 

Hereditary spinal ataxia I have discussed in the next section. 

Under dementia paralytica these complications and sequelae will 
be referred to. 

ATAXIC PARAPLEGIA. 

This is not a disease. It is merely a characteristic syndrome which 
has many congeners and which is the result of a combination oi two 
diseases, or rather sets of symptoms dependent upon a lesion in both 
the lateral and posterior columns of the cord. It may beneficially be 
adopted as a model for the description of the general symptomatology 
of these combined scleroses and for pointing out the possible variations 
that may occur in the clinical picture of some other forms of the com- 
bination. For tile nonce then I will discuss it as though it were a 
unique and distinct entity. 

Etiology. — Heredity of some sort probably plays a role in all 
of these cases. In most of them it may amount to a mere neuropathic 
predisposition, a congenital weakness, lack of resistive power to inju- 
rious influences in certain tracts or neurones. It may be so decisive, 
as in the six cases observed by Dana, as to almost warrant Its con- 
sideration as a separate disease under the head of hereditary or familial 
ata.vie paraplegia. Dana's cases ware all women and began between 



440 THE NEURONIC DISEASES 

the ages of twelve and sixteen. Most cases begin between thirty and 
forty years of age and appear in the male sex. Absence of a history 
of syphilis or alcoholism is a striking feature. No exciting cause is 
known, though it has followed exposure to cold, sleeping in clothes 
saturated with perspiration, sexual excess, severe concussion of the 
spine and certain cachexias. I have seen the symptoms follow a severe 
anaemia and a chronic diarrhoea of twenty years' standing. Whether 
pernicious anaemia produces a systemic sclerosis in the lateral and pos- 
terior columns or merely a diffuse myelitic condition is not yet posi- 
tively settled. Lichtheim, Norine, Minnich, v. Xoorden, Taylor, Water- 
man and Billings believe that it is a diffuse process. Oppenheim still 
believes that it is a true combined systemic neurone disease. Taylor 
and Waterman, Bastianelli, Russell, Batten and Collier, Billings and 
others consider that the arteriosclerosis, the anaemia, and the other 
concomitant conditions observed in these cases of combined degenera- 
tion in the cord are the result of the same general toxaemia that gives 
rise to the spinal lesion and are not themselves the direct cause of the 
latter. 

Little as we know about the etiology of these combined degenera- 
tions, be they diffuse or systemic, two factors seem to stand out with 
suspicious prominence, namely, an inherited predisposition and a 
toxcemic excitation. 

Pathology and Pathogenesis. — The essential lesion is a degen- 
erative sclerosis of the posterior and lateral columns of the cord. It 
may extend throughout the entire length of the cord, though the pro- 
cess is apt to be more pronounced in the thoracic region. In some in- 
stances, as for example Friedreich's disease, the degeneration is 
sharply limited to certain tracts, notably the postero-median, postero- 
lateral and crossed pyramidal, and the disease is shown to be a purely 
systemic one. In other instances, as for example the anaemic cases 
(Bastianelli, Russell, Batten and Collier, Spiller and others) the lesion 
is less sharply defined and the disease process may be regarded more 
as a diffuse one. It may be that secondary degenerations of a systemic 
character follow and are associated with the diffuse lesions in many 
of the cases, thus accounting for their general systemic appearance 
upon post mortem examination. 

Other tracts besides Goll's, Burdach's and the crossed pyramidal 
that sometimes participate in the degeneration are the direct cerebellar, 
the anterior or direct pyramidal and the antero-lateral. The gray mat- 
ter of the cord, the spinal roots and the anterior root zones are not 
implicated. The membranes have only rarely been diseased. 

The sclerosis is of the ordinary type though its distribution and 
intensity are subject to considerable variation in the respective columns 
where it appears. In the laterial columns it is always less systemic 
in its limitations than it is in the posterior columns : and usually there 
is a narrow strip of healthy tissue immediately adjoining either side 
of the posterior horns. Tn the severe anaemic and toxic cases there 
may be such a rapid destruction of the neurones that a peculiar perfor- 
ated appearance is given to the cross section of the cord. Tn such cases 



THE NEURONIC DISEASES 44I 

an oedematous condition with destruction of the septa and the forma- 
tion of granule cells may be observed (Dana). 

To sum up then, the pathology of the combined scleroses indicates 
two great groups of cases, the systemic and the diffuse, with the chief 
foci of disease in the posterior and crossed pyramidal tracts. Outside 
of Friedreich's disease and the spinal sclerosis of general paresis, 
which are purely systemic, no sharp differentiation can be made. Some 
cases are doubtless systemic from the start, others are diffuse but be- 
come later on systemic on account of the secondary degenerations. 

Symptoms. — In analyzing the clinical presentation of these cases 
of combined degeneration as seen in the cord, it must be remembered 
that we are dealing with two somewhat diametrically opposed sets of 
symptoms. In the one a spastic spinal paralysis due to degeneration 
of the pyramidal tracts is combined with a true ataxia, lancinating 
pains, pupillary rigidity, bladder trouble and other tabetic symptoms; 
in the other the symptom-complex of tabes is accompanied from the 
beginning by motor weakness. 

Studied separately the clinical manifestations of lateral degener- 
ation would, a priori, seem to neutralize those of posterior degenera- 
tion. And yet such is not strictly the case. There is never a com- 
plete annihilation of one set of symptoms by the other. One may be 
more prominent than the other and thus determine the leaning of the 
case toward spastic paralysis or locomotor ataxia. Whichever the dis- 
ease seems to tend toward, always search for indications of the other. 

Like the lesion, therefore, the symptomatology of these cases is 
always a combination. This, however, does not express the whole 
truth, for there is more than a mere combination of symptoms, there 
is a more or less characteristic modification wrought in the clinical pic- 
ture by the simple combination. It is the relative constancy of these 
characteristic modifications of the symptomatology in toto that has 
led to not a little confusion in the past and betrayed writers into estab- 
lishing new diseases out of the various clinical presentations. Inter- 
mediate types are here so numerous, and the gradations from one to 
the other are so gradual, that no description will stand rigidly for 
all types. The ataxic paraplegia of Gowers, while not a fixed type, 
will answer well enough as a basis for a general description of the 
symptomatology of the combined sclerosis, the description to be always 
modified to suit the etiology, age of patient and prominence of the loca- 
tion of the lesion in the particular case in hand. 

Usually the symptoms appear slowly. There is weakness in the 
legs for several months or years and then the walking becomes grad- 
ually impaired. The weakness and incoordination may be confined to 
the legs, though it is not infrequent that they extend to the arms. Ex- 
ertion, turning, walking in the dark become arduous. Examination 
reveals even at this time a real condition of paresis in the muscles. < tae 
leg, one set of muscles may be implicated more than another. The 
gait resembles that of tabes but the high elevation of the leg and tin- 
stamping of the heel on the floor are not so marked as in tin- latter 
disease. The ataxia is both static and motor. 

In the great majority of cases the knee-jerk is markedly exagger- 



442 1HE NEURONIC DISEASES 

ated and a distinct rectus clonus can be elicited. Foot clonus is also 
generally present. This exaggeration of the patella reflex contrasts 
these cases strongly from locomotor ataxia. It continues mostly 
throughout the entire course of the disease. In the cases in which the 
knee-jerk is at first increased, and later annulled, the degeneration in 
the posterior columns has descended into the lumbar region. The case 
then resembles mOre nearly tabes but differs from it in manifesting a 
true progressive motor weakness or paresis. 

The marked absence of sensory symptoms also distinguishes these 
cases from tabes. Lightning pains are scarcely ever observed. Some- 
times dull pains occur in the legs, in the spine and around the body. 
As a rule cutaneous sensation is unaffected. Hyperesthesia has been 
rarely noted. I have seen the cutaneous reflex of the sole of the foot 
highly exaggerated, especially in the anaemic cases. The tickling was 
not distressing to the patient though the limb was violently drawn 
up. The cremasteric and abdominal cutaneous reflexes may be lost at 
times. In exceptional instances the sensory phenomena may be as 
positive as they are in tabes. These are the cases in which the knee- 
jerks are lost and the tabetic resemblance is marked. According to 
Gowers these intermediate cases between ataxic paraplegia and true 
tabes do not constitute more than five per cent, of all the cases with 
ataxia and motor weakness. 

The muscles are not wasted to any extent and the electrical re- 
sponses are normal. 

Sexual vigor may be lost early. The sphincters are usually im- 
paired but only moderately. 

The eye symptoms when present are the same as those met with 
in tabes. They are less frequent, however, than they are in the lat- 
ter disease. Nystagmus does not occur generally ; though with other 
bulbar symptoms it is a positive feature in Friedreich's hereditary tvpe 
of combined sclerosis. 

Articulation is slightly impaired in some cases. Gowers says it 
is not uncommon. A slight amnesia as a rule is all that character- 
izes the mental state in the way of deterioration. 

As the disease continues to advance the paresis becomes more and 
more marked until it quite overwhelms the incoordination. Finally 
after a period of going: about on crutches, the patient takes to his bed 
never to leave it. Stiffness and rigidity in the muscles increase and 
even before becoming bedridden the case develops into one of spastic 
paraplegia. The arms are now involved, if they have been fortunate 
in escaping so far. At length complete paralysis comes on and the 
case terminates as spinal spastic paralysis usually does. To the end 
sensation usually remains unimpaired, crises are absent, and the re- 
flex action of the iris, unless lost early, remains normal. 

Among the complications are dementia paralytica with its array of 
mental symptoms, occasional slight muscular atrophy and arthritis. 

Such in the main is the clinical picture of ataxic paraplegia, or 
combined sclerosis of the posterior and lateral columns of the cord. 
The differences to be observed in the symptomatology of. and the prob- 
able reasons for those differences in. the combined sclerosis of Fried- 



THE NEURONIC DISEASES 443 

reich's ataxia and dementia paralytica will be pointed out when these 
diseases are discussed. 

Some other modifications, not sufficient to constitute the basis for 
the establishment of new diseases, may perhaps be profitably referred 
to here. 

In hereditary ataxic paraplegia there is stiffness and weakness in 
the legs and the ataxia is more cerebellar in type than spinal. Re- 
flexes are exaggerated. There is some paresthesia. The arms are 
only slightly involved. Optic neuritis was present in one case. The 
sphincters are intact, the mind is clear and the prognosis is more fav- 
orable than in Friedreich's disease. Xo autopsy having been made 
the true nature of these cases is not determined. They may be re- 
lated to Friedreich's ataxia or to Marie's hereditary cerebellar ataxia. 

In the anaemic and toxic cases of combined sclerosis there are apt 
to be early sensory symptoms chiefly of a paresthetic character. 
Numbness, pain and anaesthesia may appear in ail four extremities. 
Gradually the motor weakness comes on and finally the paraplegia. 
These are associated with the ataxia. Spasticity, exaggerated knee- 
jerks, ankle-clonus are all present. The mind is weakened toward the 
end. Severe anaemia, diarrhoea, emaciation are all concomitant mani- 
festations suggestive of a profound toxemic condition. 

Diagnosis. — Enough has been said under the head of symptoms 
to indicate the differential diagnosis of a combined sclerosis from sim- 
ulated diseases. Locomotor ataxia on the one hand, and spinal spas- 
tic paralysis on the other, are the affections most likely to cause con- 
fusion. In tabes the patella reflex is always and earl}' lost ; it is usu- 
ally exaggerated in the combined disease. The sensory and pupillary 
phenomena are as a rule sufficiently different in the two diseases to g< i 
a long way in establishing the differential diagnosis. In primary spas- 
tic paraplegia there is no ataxia. As Gowers says epigrammatically, 
ataxic paraplegia is spastic paraplegia plus incoordination. The hered- 
itary and familial types of combined sclerosis are distinguished by 
their history, the age of the patient and the repetition of the disease in 
the same family. Myelitis is sometimes hard to distinguish, and in fact 
Oppenheim declares that the toxemic ca*ses, while svmtomatically allied 
to the combined scleroses, are pathologically related to myelitis. Mye- 
litis, however, is regressive, though of course it may set up a 
ondary progressive defeneration in the lateral and posterior tracts. 
Such cases cannot be differentiated. Cerebellar tumor may cause symp- 
toms resembling ataxic paraplegia, but the headache, vertigo, optic 
neuritis and other well known signs of an intra-cranial neoplasm are 
present to aid in the diagnosis. 

Prognosis. — These degenerations are incurable. They are chronic 
and progressive in their course. Sometimes they remit symptomatically 
for a time but the onward course of the disease is again resumed. The 
danger to life is not great. Kidney disease and bedsores are the ac- 
cidents most to be dreaded as these, or general exhaustion, usually 
close the scene. Improvement has occurred and life been prolonged in 
a few cases. Very exceptionally a cure has been observed. The pr 
nosis therefore as to life is fair; as t<» recovery had. 



444 THE NEURONIC DISEASES 

Treatment. — The treatment is the same as that for tabes and 
spastic paraplegia, the two diseases out of which, as it were, ataxic 
paraplegia is framed. It is no less and no more satisfactory than it 
is in them. The etiology, especially in the anaemic and toxic cases, 
and the symptoms, are the chief points of attack in the therapeutic man- 
agement of ataxic paraplegia. 

HEREDITARY ATAXIA. 

Under the broad term hereditary ataxia are included several forms 
of degenerative disease of the central nervous system, particularly of 
the cerebellum and spinal cord, in which etiologically heredity plays a 
dominant role and symptomatically ataxia stands forth as a- leading 
phenomenon. 

Three types of hereditary ataxia are recognized, namely, Fried- 
reich's ataxia, hereditary ataxic paraplegia and hereditary cerebellar 
ataxia. 

There will doubtless come others. 

The exact relationship of these troubles to one another is not 
clear, though there is such, since they overlap, to a certain extent, both. 
symptomatically and pathologically. The last is primarily an atrophic 
disease of the cerebellum, with certain secondary changes in the cord. 
I will refer to it more in detail elsewhere. The other two are often 
regarded as diseases of the spinal cord. Their principal lesion seems- 
to be spinal though there are frequent intra-cranial manifestations 
which link them together and give them both a sort of connection 
with the cerebellar type of hereditary ataxia. 

In one thing they all agree, namely, in being dependent primarily 
upon an inherited developmental defect, on account of which the sys- 
temic degeneration occurs in certain encephalo-spinal tracts. 

Before a more accurate classification of these various types of 
hereditary ataxia can be made, more definite data will have to be forth- 
coming in regard to their pathogenesis. 

For the further description of hereditary cerebellar ataxia the 
reader is referred to the section on diseases of the cerebellum. 

FRIEDREICH'S DISEASE. 

It was in 1861 that Friedreich first described the disease that now 
bears his name. It is a rare affection, though upwards of two hun- 
dred cases have been so far reported. Our knowledge of it has been 
increased by the labors of Fere, Mobius, Cuche, Ormerod, Bury, Sep- 
pilli, Vizioli, Ladame, Griffith, Burr and others. 

Heredity and ataxia are the cardinal features of the malady, 
though there are many other characteristics that serve to identify the 
particular form of hereditary ataxia which Friedreich described. Of 
the various names that have been given to the disease from time to- 
time all have proved to be defective and misleading; hence, objection- 
able as it is to name an affection after a man, in this particular in- 



THE NEURONIC DISEASES 445 

stance, it is almost necessary to do so until the pathology and noso- 
logical position of the trouble is more definitely established. 

Etiology. — Heredity is the predominant factor in the etiology 
of this disease. It is both direct and indirect. In the broadest sense, 
therefore. Friedreich's disease is a family disease, a characteristic 
which stamps it at once. In a goodly number of cases one or more 
ancestors of the patient have been afflicted with the same malady. 
Sometimes it can be traced through four generations, increasing in 
•extent and intensity as it passes on down through the family. Often 
several members of the same family and generation are attacked. The 
heredity is not always direct. In the remaining cases it is indirect and 
seems to follow some neurosis or profound nervous strain in the fore- 
bears. This indirect heredity is much more frequently traceable than 
is the direct. The disease therefore is in all likelihood the result of 
an inherited defect of a developmental and neuropathic character. In 
the parents we find the following influences at work : neuropathies, 
such as epilepsy, psychoses, great nervous irritability ; alcoholism ; tu- 
berculosis ; syphilis ; consanguinity, and other unclassified cachexias 
and constitutional abnormalities. The hereditary influence need not 
necessarily be obvious in the parents, for in some cases they have been 
healthy and sound. In such instances somewhere among the blood 
relations will the taint be found lurking. In some cases the disease 
has been precipitated by an infectious fever, notably typhoid, pertussis, 
variola, meningitis, periostitis, measles, scarlatina, rheumatism and 
probably diphtheria. This form of ataxia never follows tabes dorsalis 
either in the parent or in the patient himself. If it does it must be 
exceedingly rare. 

Though the affection is hereditary and familial, it is rarely seen 
before the seventh or after the forty-fifth year of age. A large number 
of cases develop about the age of puberty. After twenty it rapidly 
becomes more and more rare. The majority of the cases make their 
appearance between the ages of six and ten. In fact, roughly speaking 
the age of ten is the time to expect its onset. It has been seen in a 
number of instances as early as two years of age. Most authors de- 
clare that it manifests no marked preference for either sex and yet 
in Griffith's T43 collected cases the percentage of males was almost 
double that of females. Dana says that in America, where more cases 
have been observed than in any other country, the females outnumbei 
the males in the ratio of three to two. The laboring and agricultural 
classes, rather than the denizens of the crowded cities, include chiefly 
the parents of these children. In some instances the outbreak of the 
disease has been attributed to falls and other traumata, child-bearing 
lactation and similar depressing factors. 

Pathology and Pathogenesis. — Much discussion has been ex- 
pended upon the pathology of the disease and this is not to be won- 
dered at. It is the most interesting feature about it and necessarih 
underlies its correct nomenclature and nosological position. Clinicalh 
the disease seems to be intermediate between tabes dorsalis and dis- 
seminated sclerosis, having several of the leading symptoms of both. 
Pathologically, however, it is related to Growers 1 ataxic paraplegia or 



446 



THE NEURONIC DISEASES 



the combined scleroses of the lateral and posterior columns of the cord. 
Seppilli, Brousse, Charcot and others regard it entirely as a distinct 
and independent malady. 

Constant lesions are found only in the spinal cord and medulla. 
The brain and nerves remain intact or are so very rarely implicated 
as to be excluded from consideration. 

The cord is generally smaller than normal throughout, and some- 
what flattened laterally and posteriorly. Along the posterior surface 
there are indications of a chronic leptomeningitis. The characteristic 
and constant finding in the cord is a systemic degeneration, involving 
the posterior columns, the postero-lateral cerebellar tracts and, to a 
lesser degree perhaps, the crossed pyramidal tracts. Gowers' tract is 
sometimes included. The change extends the entire length of the 
cord, though it is as a rule most pronounced in the lumbar region. 
Goll's columns are completely hardened ; Burdach's almost entirely so^- 

FIGURE 90. 




Cross-section of the spinal cord in Friedreich's disease. Pal's stain. (Alter 
Marinesco and Oppenheim.) 

A trace of healthy tissue sometimes lies between Burdach's column 
and the posterior horn. The crossed pyramidal tracts are always, and 
quite completely, sclerosed. The process seems to be more diffuse in 
the lateral columns, leaving a slip of healthy tissue alongside of the 
posterior horn, and rarely or never extending in front of a line drawn 
transversely through the middle of the cord. In a large number of 
cases the disease implicates the direct cerebellar tract, and the ascend- 
ing antero-lateral tract. Rarely are the anterior median columns in- 
volved. The anterior root-zones and the gray matter are normal. All 
the nerve-roots may be hardened, the anterior much less frequently 
than the posterior. The peripheral nerves are not regularly involved. 

The central canal of the cord has been seen to be inflamed in 
some instances and there have been present distinct but small cavities. 
The cells of Clarke's columns are often shrunken and without pro- 
cesses. Degeneration ^\ the posterior horns has been observed. 

In the medulla are Found traces of the upward extension of this 
sclerosis, the hypoglossal nucleus portraying the most significant 
change. 

The interpretation that is to be given all these findings is still 
largely hypothetical. If we exclude rigidly those cases in which some 



THE NEURONIC DISEASES 447 

change in the cerebellum has been observed we find ourselves confronted 
by a spinal cord disease apparently. In a sense it is a systemic affec- 
tion but the lesion does not confine itself, especially in the lateral col- 
umns, within sharp outlines in any one tract. There is a certain de- 
gree of diffuseness that nullifies all idea of the degeneration being sec- 
ondary to some brain lesion in the larger number of cases at least, 
and the view is strengthened that Friedreich's disease is a primary 
sclerosis of the cord tracts. The similarity of hereditary syphilis and 
Friedreich's ataxia lends support to this conception. When we attempt 
to follow the many explanations ottered by various investigators at 
different times to determine the real pathogenesis of the disease, the 
original focus of the disease process, and the connection of the many 
pathological findings with one another, we find ourselves tossed about 
on a sea of theories and hypotheses. 

The only theory worth considering is the one which refers the 
whole trouble to an inherited defect in the cerebellum. This theory 
promulgated by Hammond has been lately revived and vigorously sup- 
ported by Menzer, Nonne, Auscher, Senator and others. The post mor- 
tem findings, however, in the cerebellar tissues are far from being con- 
clusive. 

Marie's hereditary cerebellar ataxia is probably an entirely differ- 
ent trouble and is not to be confused with the cerebellar theory of 
Friedreich's ataxia just referred to. The insignificance of the changes 
in the cerebellar cortex, their great rarity, as well as the constancy 
and character of the spinal cord changes, all incline me to believe that 
in Friedreich's disease we have a combined degenerative sclerosis of 
the posterior and lateral columns, with their related structures. It is 
probably developmental in origin in most cases, certain congenitally 
weak neurones succumbing under various exciting influences. In 
other words the disease in my judgment approaches very closely to 
being a congenital or hereditary ataxic paraplegia. 

The pathological process being in advance in the posterior col- 
umns, the symptoms arc largely ataxic in character, to such an extent 
even as to cause the disease to closely resemble locomotor ataxia. 

To put it in another way, Friedreich's disease, in its present form, 
is the hereditary or congenital analogue of those cases of ataxic 
paraplegia or combined sclerosis in which the ataxia, absent knee-jerks 
and other manifestations, ally it, symptomatically at least, with tabes 
dorsalis. 

The cases which have been reported as cases of hereditary ataxia 
and connected with Friedreich's disease, such as those of Sanger 
Brown, Dana and others, in which the reflexes have been exagger- 
ated, and which have been called hereditary ataxic paraplegia, are 
also inherited <>r congenital types of combined sclerosis of the lateral 
and posterior columns in which the disease i>n>ee>s i n the lateral col- 
umns is far in advance of that in the posterior. 

If this conception of Friedreich's disease and of hereditary ataxic 
paraplegia should ultimately prove to be the correct one, both 
will fall under the general classification of ataxic paraplegia or com- 
bined sclerosis of the lateral and posterior columns. The difference 



448 THE NEURONIC DISEASES 

between these and the ordinary form of the trouble is dependent 
upon the hereditary origin of the former, while the difference between 
each other is the result of the relatively greater severity of the dis- 
ease process in the lateral or the posterior tracts. 

Symptoms. — Ataxia is not only the earliest, but it is the domi- 
nant symptom throughout the entire course of the disease. It usually 
attacks the lower limbs first and the upper limbs later. The reverse 
occasionally takes place. Before the ataxia is fully established there 
are generally preceding symptoms, such as weakness, unsteadiness, 
oscillation and staggering in the gait, even frequent falling. The 
ataxia is not exactly like that of tabes, jerky, irregular, with stamping 
of the heel first. It more nearly resembles a disturbance of equilibrium, 
a cerebellar ataxia, for which reason Charcot used to speak of it as a 
demarche tabeto-cerebelleuse. It is marked even when the patient is 
standing still. It is not increased, however, by closing the eyes, prob- 
ably because the early age of the patient is such that he has not ac- 
quired the habit of using his eyes yet in maintaining his equilibrium. 

As I have intimated the characteristic differences between the 
symptoms of this disease and tabes are due to the associated degenera- 
tion in the lateral columns and the occurrence of the disease in young, 
undeveloped individuals. 

Eclampsia and hysterical attacks have preceded and accompanied 
the ataxia in a few cases. In many there are painful, cramp-like 
spasms in some of the muscles. The face, neck, hands and feet have 
thus been involuntarily contracted. Tremor, not of the intentional 
type, but rather simple oscillations, is not infrequent in various parts 
of the body. Choreiform movements are almost constant in accom- 
panying the ataxia and may appear in any group of muscles. In ad- 
vanced cases decided weakness and more or less paralysis are com- 
mon features. The gait, which has been difficult from the first on 
account of the incoordination, later on becomes so affected that walk- 
ing is an absolute impossibility, and the patient keeps to his bed. The 
paralysis and subsequent contractures add to this unfortunate condi- 
tion. In many cases curvature of the spine takes place and marked dor- 
sal flexion of the toes. Talipes, chiefly of the equino-varus type is 
frequent. The knee-jerks are lost in pure cases of Friedreich's ataxia, 
which is a most important indication of the disease. In the few cases 
in which they have been exaggerated, the trouble was probably of 
cerebellar origin. Exceptionally ankle-clonus has been observed. The 
cutaneous reflexes are all intact or only very rarely altered. As there 
are scarcely any sensory manifestations the ataxia and the altered ten- 
don reflexes cannot be attributed to them. The muscles are not typ- 
ically atrophied, though there may be some slight wasting late in the 
disease. Their electrical contractibility is not in the least modified. 
Coldness of the surface of the body, cyanosis, oedema, chilblains, thick- 
ening of the skin, development of adipose tissue and even bedsores 
have been reported as among the rare vasomotor and trophic symptoms, 
and as particularly late in the disease. 

Sensory symptoms are not entirely wanting though they are so 
rare as to justify the general statement that sensation is normal in 



THE NEURONIC DISEASES 449 

Friedreich's disease. The absence of the characteristic pains of tabes 
distinguishes it. And yet headache has preceded and accompanied the 
ataxia. When the disease is well established, occasional dull pains are 
noticed elsewhere. There may be tenderness over the spine. The 
muscles may be subjected to painful cramps. Pains in the articulations 
have been complained of. The cutaneous sensibility is not generally 
involved. Formication, tingling and numbness may be present and 
even anaesthesia. The muscle-sense is usually intact. 

Disturbance of the speech is a frequent trait and is one of the most 
prominent of the bulbar symptoms. It is generally a late symptom 
and appears about the same time as nystagmus, another most impor- 
tant symptom. It is a true dysarthria. The speech is slow and labor- 
ed, irregular and mangled. Sometimes it is rapid and slurring, typic- 
ally scanning, jerky, or confluent. The trouble may at times be very 

FIGURE 91. 




Position of the great toe and condition 
of the foot in Friedreich's disease. (After 

Tlriccn.nH \ 



Brissaud.) 

marked. At other times it is scarcely noticeable. On account of the 
rushing, tumbling character of it Seeligmuller spoke of it in one of 
his cases as an "ataxia of thought," as the patient seemed to begin a 
new sentence before finishing the old one. The tongue frequently ex- 
hibits a tremor, an oscillatory movement and a peculiar curling and 
uncurling. Mastication and deglutition are not generally affected. 

The chief eye symptom is nystagmus. Though this is a late symp- 
tom it is a most significant one. It is less common than the speech 
disorders, though the two usually appear together. Static nystagmus 
has been observed in a few cases. Strabismus has been mentioned and 
also a slight degree of ptosis. The pupillary reactions and the vision 
are undisturbed in the vast majority of cases, which again distinguishes 
Friedreich's ataxia from tabes dorsalis. The changes in the color 
fields and the blindness that have been noted have been SO rare that 
they probably represented some complication. 

The mental faculties are but little affected, a feature of Fried- 
reich's disease which helps to differentiate it from disseminated sclero- 
sis. There may be some amnesia and in rare instances an arrest of 



45^ THE NEURONIC DISEASES 

mental development. Vertigo is rather a frequent symptom, occurring 
both early and late in the disorder. It may be associated with mere 
giddiness, fainting or actual loss of consciousness. It may come on 
while the patient is standing or reclining. 

Visceral, secretory and sexual disorders are rare and are probably 
mere accidents. 

Diagnosis. — The essential points to be noted in the diagnosis of 
Friedreich's form of hereditary ataxia are the hereditary and familial 
character of the disease, the early age at which the symptoms first 
appear, the peculiar ataxia starting in the legs and extending to the 
arms, the speech disturbances, nystagmus, curvature of the spine, 
talipes and late paralysis. With these symptoms it is also to be noted 
that usually the patella reflexes are lost, sensory symptoms are absent 
or very slight, trophic phenomena are not marked, vision and the eyes 
generally are intact, the intellect is clear, and the visceral and circu- 
latory systems show no disorder. 

The two diseases with which Friedreich's ataxia is liable to be 
confused are tabes dorsalis and disseminated sclerosis. Locomotor 
ataxia follows a history of syphilitic infection and appears later in life. 
It does not reveal any direct heredity and only slightly an indirect. It 
is very exceptional for the offspring of tabetic parents to suffer from 
Friedreich's disease. Tabes is to be distinguished by the more char- 
acteristic ataxic gait, the increase of Romberg's phenomenon when 
the eyes are shut, the marked pains and other sensory symptoms, the 
crises, the constant loss of the knee-jerk, the. Argyll-Robertson pupil, 
optic atrophy and the more prominent late arthritic and other trophic 
symptoms. 

Ataxic paraplegia is an adult disease, occurring usually between 
the ages of thirty and forty. It does not appear like Friedreich's dis- 
ease in several members of the same family. The patella reflexes are 
exaggerated, nystagmus is wanting and there is no marked speech 
trouble. It is to be remembered, however, that Friedreich's malady is, 
like ataxic paraplegia, a mere combined sclerosis of the posterior and 
lateral columns. The differences between the two are the result of 
the differences in the ages between the two sets of patients, the heredi- 
tary influence, and the greater intensity of the disease process in the 
one or the other column of the cord. 

Some cases of Friedreich's disease reveal cerebral and cerebellar 
symptoms. Indeed it has been thought by some, that the primary trou- 
ble originates in the cerebellum. They are not typical cases, however, 
though at times it is extremely difficult to differentiate them. 

Simple developmental inhibition of the cerebellum, an agenesis, 
such as Marie has described, can but rarely be separated. And yet in 
these rare cases the reflexes may be exaggerated, the ocular muscles 
may be paralyzed, the pupils may be rigid, the vision affected and the 
deglutition markedly disturbed. 

Tumor of the cerebellum produces headache, optic neuritis, ver- 
tigo, vomiting and epileptiform attacks. The gait is "drunken" and is 
distinctly cerebellar. There is no spinal sclerosis and other deformities 
such as are observed in Friedreich's trouble. 



THE NEURONIC DISEASES 45 1 

Disseminated sclerosis sometimes can scarcely be differentiated, 
especially when the nystagmus, tremor and speech disorders are pres- 
ent. Multiple sclerosis is an adult's disease, however, developing usu- 
ally after twenty, it is not under hereditary influence, and it progresses 
remittently. The nystagmus is marked and the speech is more scan- 
ning in character than it is in hereditary ataxia. Other distinguishing 
symptoms of multiple sclerosis that aid in the differential diagnosis are 
exaggeration of the knee-jerks, the ankle-clonus, the intentional tre- 
mor, the rhythmic oscillations, the rigidity and spasticity of the limbs, 
the disturbances of the intellect, and the epileptiform and apoplecti- 
form attacks. 

Prognosis and Course. — Friedreich's disease is a chronic and 
progressive affection. It may last twenty, thirty or forty years. It 
never remits, though at times it seems to cease progressing for a while. 
The symptoms may abate and thus raise false hopes of a cure. The 
patient, as a rule, ultimately becomes bedridden and dies of nephritis, 
decubitus or some intercurrent malady. In regard to the duration of 
life the prognosis is favorable ; in regard to cure it is absolutely bad. 

Treatment. — There is no direct treatment known that will mod- 
ify the progress of the malady. Tonics are always in order, of course, 
as well as good regimen and proper hygiene. Nitrate of silver, arsenic, 
phosphorus, iodine, zinc, have all been tried and found wanting. In 
one case the constant current applied to the spine produced some bene- 
fit. It is a measure to be used, however, very guardedly. Sympto- 
matic treatment includes electricity and massage for the weakening 
muscles, a jacket for the curvature of the spine, and the closest atten- 
tion to all the functions of the viscera. 

AMAUROTIC FAMILY IDIOCY. 

In 1896 Sachs gave this name to a hereditary disease in which 
idiocy, spastic paralysis and blindness constitute the cardinal symp- 
toms. On account of the eye trouble, Tay, in 1881, first called atten- 
tion to the cases. The first autopsy on a case was made by Sachs, in 
1887, who at that time attributed the manifestations to a simple agen- 
esis corticalis. Later on Kingdon reported an autopsy upon a case 
and was the first to attract attention to the similarity between the cases 
noted early by the ophthalmologists and those reported by Sachs. 
Cases and studies of the disease have since been reported by Claiborne, 
Patrick, Kuh, Jacobi, Hirsch, Peterson, Koplik, Cotton, Hirschberg 
and others. About thirty or more cases have now been put upon record. 

Etiology. — The affection seems to be distinctly hereditary and 
of the familial type of troubles. Peterson reported three members of 
one family afflicted with it. This would seem to declare most posi- 
tively for an inherited, rather than a mere congenital, cause, as would 
also the absence of all birth difficulties and the presence of a prog 
sive degeneration of the cellular elements of the entire nervous 
tern. The children are of the Jewish race generally, though not ex- 
clusively so. They are born normally, and at birth, and for the first 
few months thereafter, seem in every way to be healthy. The (lis- 



452 THE NEURONIC DISEASES 

order makes its appearance, however, in the first six months of life as 
a rule. 

Pathology and Pathogenesis. — The autopsies have not been nu- 
merous enough to enable us to form a definite pathology. In some 
cases the findings have suggested a simple arrest of development ; in 
others an infective process, possibly of a meningo-encephalitic type ; 
and in still others a meningitis. No vascular or inflammatory changes 
have actually been discovered and if they were at all present before 
birth they must have completely disappeared. There are no signs of 
inherited syphilis or other diathesis. Hydrocephalus of a pronounced 
character has been noted. The entire nervous system reveals a con- 
dition of progressive degeneracy. In this connection it is suggestive that 
many of these children exhibit external degenerative stigmata. 

A dispute wages around the question as to the primary or sec- 
ondary nature of the neuronic degeneration. Many pathologists feel 
that simple agenesis will not wholly account for it. There is, as Kuh 
puts it, "a distinctly retrogressive and destructive change." Hirsch 
and Jacobi suspect that an infection, possibly derived from the moth- 
er's milk, is to be blamed for the trouble. Sachs reported two cases, 
in opposition to this theory, that were not breast fed. All such ex- 
planations have to combat the apparently hereditary and frequently 
familial features of the disease. In Cotton's case, the father's cousin's 
only child died in convulsions at twenty months, blind and idiotic. I 
have mentioned Peterson's three cases in one family. 

Symptoms. — Three great symptoms stand out with special prom- 
inence in amaurotic idiocy, namely, the mental deterioration, the spastic 
paralysis of all four limbs and the blindness from optic atrophy, with a 
peculiar appearance of the macula lutca. 

During the first five or six months of life the child seems normal 
in every respect. Then it is noticed that it gradually begins to fail 
in strength, to be disinclined to move, and to show a falling off of the 
intelligence. It grows apathetic, is at times restless and silly. In some 
cases convulsions and epileptiform seizures have occurred. Gradually 
it becomes stupid with such a hyperacuity of the reflexes that a sudden 
noise or a gentle slap will cause a great start, even a convulsion. 

During these mental changes there is an increasing spastic paraly- 
sis creeping over the muscles of the body. The head and trunk can- 
not be held erect, and the voluntary movements are distinctly athctoid 
in character. The associated movements and the reflexes are all mark- 
edly exaggerated. Tonic contractions occur in the whole musculature 
upon the slightest stimulation. The general spasticity and reflex ex- 
aggerations point to profound degenerative changes in the upper mo- 
tor segment. Towards the end there is complete paralysis. 

The paralytic symptoms involve the eyes also. Nystagmus, strab- 
ismus and unequal pupils may all be expected. Amblyopia is thus 
present at first but as the optic atrophy proceeds it disappears before 
the growing amaurosis. The appearance of the optic disc is pathog- 
nomonic in this disease and has been graphically described by Tay, 
Wadsworth, Carter. Beard, Wescott and others. It is so characteris- 
tic that, as a symptom of a general disorder, it stands alone, "grand, 




PLATJO II. 



Fundus oculi in amaurotic family idiocy. Drawn 
from life. ( After Beard. ) 



THE NEURONIC DISEASES 453 

gloomy and peculiar." The atrophy of the optic nerve and retina does 
not appear to be as pronounced as one would expect. The change in 
and around the macula lutea is the absolutely diagnostic manifesta- 
tion. Beard describes it thus : Surrounding the fovea centralis, con- 
centric with it, and two or three times its size, is a liver-colored disc. 
This disc is the center of a zone of grayish-white which gradually fades 
away into the normal red-orange of the eye ground. As clear cut as 
a coin is this livid disc. It is not irregular in outline as is the case 
in acute inflammatory conditions, where the surrounding retina is infil- 
trated, nor is it cherry-red or carmine, as in those cases, but is dis- 
tinctly brownish. It is larger than the fovea ; that is to say, instead 
of marking the area which is occupied by the cones alone, it marks 
that which is devoid of the ganglion cells. The whitish zone that sur- 
rounds the center is also highly characteristic. It is nebulous rather 
than cloudy. If is almost white at the circumference of the liver- 
colored disc, thence gradually thins away to nothing, but is translucent 
and exhibits some color throughout. It does not obscure the retinal 
vessels which enter it. It only serves to make them more distinct by 
contrast, so that one is able to trace the tiniest of them right up to the 
central spot. 

In addition to those that have just been described, other symp- 
toms that have occasionally been noted in the disease are muscular 
flaccidity, tremor, normal and even subnormal reflexes, dysphagia, 
vomiting, hyperacusis and hyperesthesia. Some of the children have 
been badly nourished and rachitic. The head has been enlarged and 
the fontanelles still open. In some cases atrophy of the muscles has 
been observed in one part of the body while marked rigidity was noted 
in another part. Occasionally the tendency toward a localization of the 
symptoms, such as in a hemiplegic condition, has been strongly sug- 
gestive of a gross, focal lesion. The pulse rate is often rapid ; the 
temperature is practically normal. 

Diagnosis. — Given a case of idiocy with a general spastic paraly- 
sis and the typical appearance of the fundus oculi, the diagnosis is posi- 
tive and easy. Unless an ophthalmoscopic examination be made, the 
condition might well be mistaken for a diplcgic one due to some form 
of prenatal gross vascular lesion or Strumpell's type of meningo- 
encephalitis or polioencephalitis. 

In dealing with all of these various forms of infantile neuronic 
degenerations we are on the borderline between those that are due t<> 
mere developmental incapacity and those that owe their deterioration 
to some more gross, external influence, like hemorrhage, inflammation 
or vascular obstructions. Hence the difficulty in always determining 
the pathogenesis of these cases and the still more discouraging difti- 
culty of knowing how always to make an accurate diagnos 

On account of the heredity, and above all. on account of the 
unique ocular presentation, I am inclined to lean towards the view 
that this disease is a fundamental developmental defect, cue in which 
the newly-coined word of Gowers, abiotrophy, could be applied. 

All cases diagnosed as amaurotic family idiocy in which the 
typical eye grounds were not present, and especially all cases in 



454 THE NEURONIC DISEASES 

which focal symptoms were pronounced and not typical eye grounds 
present, would be open to very great criticism. Infantile hemiplegia 
and diplegia would be more of a probability for such cases. Without 
the typical eye ground, amaurotic family idiocy may be mistaken for 
rachitic pseudo-paralysis, cerebellar tumor, tubercular marasmus and 
congenital blindness in an idiot. 

Prognosis. — This is decidedly bad. The children all die sooner 
or later, usually in a few months or a year or two, from convulsions 
and general marasmus. Herein this disease differs from the diplegic 
cases. The early death has even been spoken of as its fourth car- 
dinal symptom, so uniformly certain is it. This again suggests to my 
mind the profound biological origin of the degeneration here, as dis- 
tinguished from the secondary degeneration that accompanies encepha- 
litic and vascular processes. It is in harmony with what I have several 
times pointed out before, namely, that the prognosis of the primary 
neuronic degenerations are almost uniformly bad ; whereas the prog- 
nosis of the vascular troubles is, comparatively speaking, good. 

Treatment. — There is no treatment for this, any more than there 
is for any of the other forms of primary, progressive neuronic degen- 
eration. 

MULTIPLE NEURITIS AND NEUROMYELITIS. 

In this place would naturally fall some of the cases of toxic and 
infectious polyneuritis and ascending neuromyelitis. The latter are 
exceedingly rare and their existence doubted by some pathologists. It 
is believed that a toxic poliomyelitic primary degeneration, rather than 
an ascending degeneration, is the pathological basis. In many of the 
cases of peripheral neuritis, the lesion is believed to be a primary de- 
generation, without any interstitial inflammation, the result of the pro- 
found toxaemia. Lesions are found of a degenerative sort in the cord 
and even in the brain in these cases, so that the view is fast gaining 
ground that these cases represent a diffuse and chronic constitutional 
or general intoxication with a wide neuronic degenerative process tak- 
ing place throughout the entire nervous apparatus. The special changes 
in the peripheral nerve filaments are .believed to be due to the dis- 
turbed nutrition in the anterior horn cells and posterior ganglia, just 
as we believe is the case in other forms of infectious trouble. We are 
not ready, however, to relinquish the idea entirely that the toxin may 
act also directly upon the nerve terminals and so provoke a local de- 
generation there. All of this of course does not preclude the idea that 
some of the polyneuritides are toxic interstitial inflammations with 
secondary neuronic degeneration. This will be referred to again un- 
der the head of multiple neuritis discussed in the section devoted to 
diseases of the peripheral nerves. 

PROGRESSIVE INTERSTITIAL HYPERTROPHIC NEURITIS 

OP INFANTS. 

This is an interesting and rare affection, described recently by 
Dejerine and Sottas, which lies between the progressive muscular 
atrophies on the one hand and the frank, interstitial neuritides on the 



THE NEURONIC DISEASES 455 

other. It seems to be a family disease and it always begins in child- 
hood. The clinical picture resembles a combination of locomotor 
ataxia with progressive muscular atrophy, so much so that Strumpeil 
believed the cases were nothing more than combinations of Fried- 
reich's disease with the hereditary peroneal type of progressive muscu- 
lar atrophy. The name indicates Dejerine's own idea, however, that it 
is a form of interstitial neuritis. The post mortem findings were a 
chronic interstitial neuritis decreasing in severity from the periphery 
to the center, and involving the posterior roots. There was also a 
sclerosis of both Goll's and Burdach's columns. Nerves were hyper- 
trophied and indurated. 

Symptomatically there were lightning pains, various sensory dis- 
turbances, an ataxic gait, sluggish pupils, myosis, nystagmus, static 
ataxia and a kypho-scoliosis. There were no electrical reactions of 
degeneration though there was a quantitative decrease in the electrical 
excitability. 



SECTION C. 



THE NON-NEURON1C DISEASES. 



Interstitial, Inflammatory Troubles with Secondary Neu 
ronic Degenerations. 



THE NATURE OF THE NON-NEURONIC DISEASES. 

In our earlier studies upon the histology of the Nervous System, 
we found that its wonderful network of neurones, making 
up the innumerable pathways along which the afferent and 
efferent impulses travel, was supported by a scaffolding, so to speak, 
of connective tissue, neuroglia, bloodvessels, lymphatics and epithe- 
lium. The neuroglia we remarked was a peculiar epiblastic tissue that 
belonged solely to the nervous system. Its function is purely susten- 
tacular and it is capable of undergoing hyperplasia and degeneration. 
An illustration of the former is the gliomata that are seen in the 
gray and white substance of the brain, the cranial nerves and the 
retina. These unique neurotic growths break down easily sometimes 
and leave huge cavities. Gliosis therefore is a degenerative process, 
affecting a special variety of extra-neuronic elements and causing 
them to press upon and infiltrate among the nerve-cells to their great 
detriment. 

Excluding the neuroglia, the extra-neuronic tissue of the nervous 
system is exactly the same as it is in every other part of the body. 
The connective-tissue elements and the changes they undergo, the 
bloodvessels and the disturbances which they are subjected to, differ 
in no respect here from what they do elsewhere. The inflammations, 
hemorrhages, neoplastic over-growths and infective processes are in 
themselves the same in the brain as they are in the lungs. A neuritis, 
as an inflammatory process, differs in no resped from an interstitial 
nephritis. An intra-cranial sarcoma is the same soli of a sarcoma that 
appears in the foot. The only thing, therefore, that makes these dis- 
eases, of the extra-neuronic type, especially interesting t<> the neurolo- 
gist is, that when they occur in the nervous system, they necessarily 
damage the neighboring neurones. The- damage is usually <>!" a me 
chanical sort and represents compression, laceration and distortion. 
This is seen in the inflammatory and hemorrhagic conditions. So 
times, however, they shut off the nourishment of the neurones. Hiis 
is observed in the embolic and thrombotic conditions. Sometimes they 



458 THE NON-NEURONIC DISEASES 

even twist, stretch and displace the neurones in such a way that they 
cannot functionate properly. This is illustrated in the infiltrations of 
the gliomata and other neoplasms. 

Whatever the nature of the trouble may be in these extra-neu- 
ronic structures, the damage of the neurones themselves is strictly a 
secondary affair. The degeneration is therefore often spoken of as 
secondary. The disease which primarily starts it, and which is a dis- 
ease entirely outside of the neurones, is very properly therefore spoken 
of as a non-neuronic disease. 

As inflammation is really a regressive process, an effort of nature 
to rid and protect herself from some noxious influence, it tends always 
to disappear as soon as the harmful agent has been banished. It is 
thus more or less of an acute and temporary process and when prop- 
erly assisted it tends always toward recovery. In this way the prog- 
nosis of the inflammatory diseases of the nervous system is favorable. 

It must not be confused with the very unfavorable prognosis of 
the neuronic degenerations, whether these be primary or secondary. 

Hemorrhages, neoplasms, etc., each have their own special prog- 
nosis, which may be good, bad, or indifferent, but which should be care- 
fully distinguished from the prognosis of the mere resulting degenera- 
tion in the damaged neurones. 

In a broad sense then, we may say that the prognosis and treat- 
ment of the non-neuronic diseases are most favorable. The outlook in 
regard to the secondary neuronic changes which these diseases pro- 
duce, will depend entirely upon how severe and destructive the pri- 
mary disease was in its action upon the neurones. 

There are all grades of disturbance that may be produced in the 
neuronic elements ; and unless one keeps this fact well in mind, he will 
find himself treating hopeless and hopeful cases all alike with the ob- 
vious consequences. If an arterio-sclerosis, for instance, is amenable 
to treatment at all, the neurasthenic manifestations that often accom- 
pany it may be made to disappear by the treatment. A neurasthenia 
that is due to a defective heredity, however, and which really repre- 
sents an actual nervous incapacity from birth, cannot be expected to 
be removed by any sort of treatment. The trouble in the former case 
was a mere secondary result of mild degree from a non-neuronic dis- 
ease. Its prognosis, therefore, was good, and its treatment satisfac- 
tory. In the latter case the trouble in the neurones is essential and 
primary ; it is a positive neuronic defect or degenerative condition ; and 
hence it is irremediable by any human agency. It is too common an 
error, and one that oft leads to pessimistic views in regard to neurol- 
ogy, to say nothing of treatment, to confound the prognosis of these 
non-neuronic diseases with the prognosis of their secondary results, the 
neuronic secondary degenerations. 

For the sake of convenience, the non-neuronic diseases are usu- 
ally divided into those of the Spina! Cord, the Peripheral Nerves and 
the Brain. That this is an artificial division is shown by the fact that 
many of these diseases implicate the whole cerebrospinal axis at the 
same time, as, for instance, leptomeningitis and disseminated sclerosis. 
As the lesion, however, is more or less focal, and as the brain and 



THE NON-NEURONIC DISEASES 459 

spinal cord have each their own localization symptoms, it is conve- 
nient to divide these diseases in accordance with these gross anatomical 
divisions. 

The order that will be followed in discussing them will begin with 
the bony encasement, taking up next the membranes, and finally the 
connective tissues and bloodvessels. At this point the neurones them- 
selves will have been reached and there will be nothing left but the 
neuronic degenerative troubles which were treated of first in the book, 
because they constitute, in their last analysis, the only true specific 
nervous diseases. 



PART I 



Non-Neuronic Diseases of the Spinal Cord. 



ANATOMY AND PHYSIOLOGY OF THE SPINAL CORD. 
SPINAL LOCALIZATION AND TOPOGRAPHY. SYMP- 
TOMS OF DISEASE OF THE SPINAL CORD. LUMBAR 
PUNCTURE. 

Anatomy and Physiology. — It is unfortunate, from the neurolog- 
ical point of view, that the artificial division of the nervous system into 
Brain, Spinal Cord and Nerves is so firmly engrafted upon the minds 
of the profession. These divisions are not made upon a neurological 
basis, but upon the bony encasements and other gross factors. Essen- 
tially, neither in anatomy nor in physiology, does the brain differ from 
the spinal cord. The cells and their inter-connections are arranged 
and functionate in practically the same way. Their processes inter- 
lace and run back and forth in such a manner between the brain and 
cord that the cerebrospinal axis is practically a unit. The nerves are 
merely the processes that connect this unit with the outlying parts of 
the body. They are not separate structures but merely extensions from 
and into the cerebrospinal organ. This cerebrospinal organ is made 
up of a series of bunches of neurone bodies and in this way carry out 
the dictum of Owen when he declares that a vertebrate animal, such 
as man is, is nothing but a clothed sum of .segments. 

The segmental character of the bony spine is obvious enough and 
indicates an evolution out of a lower or articulate form of life. The 
collections of neurone bodies, the ganglionic masses, that lie side by 
side serially all along the cerebrospinal axis, and which make up the 
so-called gray matter of the brain and cord, indicate also tin- 
mental character of the central nervous system. In the cord this is 
almost as obvious as it is in the bony spine. It Is suggested in the 
longitudinal series of spinal nerve-roots which have their origin from 
a series of super-imposed discs. In the brain the same serial disc-like 
arrangement obtains, but there it has been elaborately broken up and 



40o the non-neuronic diseases 

the ganglionic masses have been, in the course of evolutionary devel- 
opment, scattered about in order to accommodate the enormously devel- 
oped condition of these frontal ganglia within the confined space to 
which they are limited by the more slowly developing skull. 

In its essential architecture the brain is only an enormous develop- 
ment of the frontal portion of the spinal cord, and the spinal cord is 
but a series of little, primitive brains lying side by side all the way 
along the spinal canal. 

To bring about harmony of action in this series of ganglionic de- 
posits of neurone-cell bodies, the latter must necessarily be joined, at 
least physiologically, together. They are. The processes from one 
ganglionic set of cells run up and down and here and there to arborize 
around the neurone cell-bodies in the neighboring and distant gangli- 
onic deposits. Some of these processes run through the nearby 
ganglia to reach the more distant ones, and in this way constitute the 
so-called gray commissures. Some of them run along just outside of 
the neighboring ganglia, and thus constitute the white associating, 
commissural and projection tracts. The serial deposits of cell-bodies,, 
so-called gray ganglia, gray matter, gray columns, and the long and 
short processes or branches from these cell-bodies that run here and 
there to connect them with one another, the ganglionic deposits with 
one another, and the ganglionic centers with the outlying parts of the 
body, all making up the so-called white matter of the commissures and 
columns, is the essential completed structure of the central nervous 
system. 

When we employ the gross divisions of the anatomists in our 
terminology, we merely mean to say that the brain is that part of the 
series of gray deposits, and that part of the white processes, that hap- 
pen to lie within the skull above the foramen magnum ; the cord is 
that part which happens to be found within the bony vertebral column ; 
and the nerves are that part of the processes that lie between the 
cerebro-spinal axis and the outlying organs and tissues of the body. 

This is a most important conception of the nervous system to 
grasp in order to understand the symptomatology of its diseases. For 
purposes of rough localization we may conveniently speak of brain, 
cord and nerve diseases, but as a matter of fact there are no dis- 
tinctive brain, cord and nerve diseases. There are no distinctive brain, 
cord or nerve functions. All the functions, all the abnormal symptoms 
of the nervous system, are neuronic functions and neuronic symptoms. 
Tf they happen to be the functions and the symptoms of those particu- 
lar neurones that lie within the skull we call them encephalic; if of 
(hose within the cord, spinal; if of those in the outlying nerves, ueu- 
ritic. Remember, however, that there is no sharp line of demarkation 
between these. Encephalic diseases produce spinal lesions and symp- 
toms and vice versa; spinal diseases produce nenritic lesions and symp- 
toms and vice versa. The greatest convenience of this artificial di- 
vision of the nervous system into brain, cord and nerves is in localizing 
the extra-new ronic lesions that constitute the inflammations, the vascu- 
lar abnormalities, the neoplasms, etc. 



THE X0X-XEUR0X1C DISEASES 



461 



I will now discuss that part of the nervous system commonly 
called the spinal cord. 

The spinal cord, spinal marrow > medulla spinalis, is that part of 
the cerebro-spinal organ that extends from the edge of the foramen 
magnum in the occipital bone to the lower part of the body of the first 
lumbar vertebra. The section just above it is called the medulla 




--Cervical por- -Dorsal por- .—Inferior por- 

tion of the spinal cord tion of the spinal tion of the spinal cord. 
(Hirschfeld). cord (Hirschfeld), and cauda equina 

(Hirschfeld). 
1 anteroinferior wall of the fourth ventricle ; 2, superior peduncle of the 
cerebellum ; 8. middle peduncle of the cerebellum ; 4, inferior peduncle 
of the cerebellum ; 5, inferior portion of the posterior median columns 
of the cord; 6, glosso-pharynereal nerve: 7, pneumogastric ; 8, spinal 
accessory nerve ; 9, 9, 9, 9, dentated ligament : 10, 10, 10, 10, posterior 
roots of the spinal nerves; 11, 11, 11, 11, posterior lateral <ir<>,,v.- ; 12, 1:2, 
12, 12. ganglia of the posterior roots of the nerves ; 13, 13, anterior roots 
of the nerves ; 14, division of the nerves into tiro branches ; 15, lower ex- 
tremity of the cord : 16, 16, coccvgeal ligament ; 17. 17. cauda equina ; 
I-VIII. cervical nerves ; I, II, III, IV-XII, dorsal nerves ; I, Il-Y, lumbar- 
nerves ; I-V, sacral nerves. 



oblongata. At the other end it terminates in a slender filament, tlu- 
filuin terminate or central ligament. It is about eighteen inches long 
and does not quite extend to the full length of the bony canal. It- 
relation to this canal varies slightly in accordance with the flexion* 
the body. 

It is inclosed in a theca, winch is longer and larger than itself 
and which constitutes the dura mater. Two other membranes en< 



462 



THE NON-NEURONIC DISEASES 



the cord also within the dura mater and are known as the arachnoid 
and the pia mater. Between the dura mater and the bony canal is a 
space containing much fat and loose areolar tissue, and large venous 
plexuses. The arachnoid is a double membrane, the outer layer of 
which hugs closely the under surface of the dura, while the inner 
layer unites somewhat with the pia. Many delicate fibres pass from 
one layer to the other. The dural layer is regarded by many histolo- 

FIGURE 94- 

17 







—Horizontal section of the cord and its envelopes, at the middle of a vertebral body 
(Schematic). 1, Spinal cord with 2, its anterior median fissure; 3. its posterior median fissure; 
4, anterior roots; 5, posterior roots; 6. pia mater 7, ligamentum dentatum; 8, connect- 

ing fibres passing from the pia to dura mater; 9, visceral layer and 9', parietal layer of the 
arachnoid 10, subarachnoid space; 11, arachnoid cavity; 12, dura mater 13, 

periosteum; 13', external periosteum; 14, cellular tissue situated between the dura mater and the* 
wall of the vertebral canal; 15, common posterior vertebral ligament; 16, intra-spinal veins; 17> 
vertebra in section. (Testui.) 

gists as the arachnoid. The space beneath it then becomes the sub- 
arachnoid space and contains the cerebro-spinal fluid and is in direct 
connection with the lymph paths of the peripheral nerves and with the 
subarachnoid space of the brain. The pia mater is a highly vascular, 
lace-like membrane which closely invests the spinal cord and sends a 
thick, fibrous septa into the anterior fissure. It is important to note 
this, as certain differences between the diseases of the anterior and of 
the posterior parts of the cord are probably due in part to this arrange- 
ment of the pia and the corresponding difference of blood supply. 
With its investing pia mater, the cord swings within the subarachnoid 
space and cerebro-spinal fluid, being suspended from above and kept 
in position by the tooth-like ligamentum dentation that fixes it at 



THE NON-NEURONIC DISEASES 463 

various points to its sheath and by the spinal nerve-roots that cross 
to reach the various intervertebral foramina. 

The cord is not of the same thickness throughout. In the upper 
part is the cervical enlargement where the great nerves of the arms 
come off, extending from the upper limit of the cord to about the 
first or second dorsal vertebra, while in the lower part is the lesser 
lumbar enlargement, where the nerves of the lower extremities orig- 
inate and extending from the tenth dorsal vertebra down to its greatest 
width opposite the twelfth dorsal vertebra on to its final tapering into 
the thin conns medullar is. 

Above the nerve roots pass almost horizontally across the sub- 
arachnoid space ; in the mid-dorsal region they incline strongly down- 
ward and thus run for a short distance obliquely across the space ; 
in the lumbar and lower regions they become almost vertical and 
run quite a long distance beside the cord before they pass out through 
their respective foramina. This is to be carefully noted as having a 
most important bearing upon clinical localization of the lesions within 
the cord. This mass of almost vertical nerve-roots hanging round 
about and concealing the terminal, central ligament of the cord con- 
stitutes the cauda equina, or horsetail. The Alum terminate is a pro- 
longation of the pia mater, inclosing for about a half of its length 
the lower end of the central canal of the cord. In the portion below the 
canal there are connective tissue, blood vessels and three or four 
minute bundles of medullated nerve fibres, some of which have a 
few ganglion cells attached. According to Rauber these represent 
rudimentary coccygeal nerve-roots, but they have no real connection 
with the proper coccygeal nerves. 

Superficially the cord is seen to be longitudinally divided by 
fissure-like depressions, along which emerge the nerve-roots. As the 
nerve-roots form themselves on each side into an anterior and a 
posterior set, the cord is thus grandly divided into anterior, lateral and 
posterior columns. The anterior column is again divided into two 1>\ 
the anterior median fissure into which dips the pia mater. The pos- 
terior column is also divided into two by a so-called posterior median 
fissure, which is not a true fissure, but merely a septum of connective 
tissue and blood vessels projected down into the cord from the pia 
mater on its surface. Thus each half of the cord has an anterior 
column in front of the anterior nerve roots, a later column between 
the anterior and posterior nerve-roots and a posterior column behind 
the posterior nerve-roots. We now begin to see thai the cord is a 
bilateral organ or represents two sides of the nervous system, identical 
in all respects. This is further demonstrated most beautifully when 
a transverse section of the cord is made and the ends of the section 
are examined. If we were to unite the- anterior and posterior median 
fissures with one cut of the knife longitudinally we would have the 
two halves of the cord separated, but presenting exactly the same 
picture. 

Before taking up the description of the inner appearance of the 
cord, it may be well to devote a paragraph to its blond supply. The 
upper part of the cord is nourished by branches from the vertebral. 



464 



THE NON-NEURONIC DISEASES 



ascending cervical and superior intercostal arteries. The lower part 
receives its supply of blood from the dorsal intercostal, lumbar and 
sacral arteries. These all send off branches which penetrate the inter- 
vertebral foramina and are finally spread out on the pia mater and the 
cord. The anterior and posterior spinal arteries run along the cor- 



FIGURE 95 (A). 



Format ret /'cut \ 




First Cervical. 

Tntermed^ cells 
Fasc ct/neat* 
Faifc. grac ///j N. 



Second Cervical. 



Clark's Coh 
Su6st. gelatin 
etttr. 

Subst. gefatm. \ r, j- s 
Col. post. 



'^termed. Cells 
~Pott Toot* 




Cent, canal 1 Mnz.rvot Fissum at%t . 

Comml3.ee/ts Csmm,ss. cetl^ 

Med. motor cells -JKotor tells 

Zat. motor cells Lateral horn 

Sixth Cervical. First Dorsal. 

—Showing Arrangement op Gray and White Matter at Different Levels 
op the Cord (After Merkel). 

responding surfaces of the cord and send off everywhere small 
branches. The branches from the intercostal, lumbar and sacral 
arteries communicate laterally with the branches from the anterior 
and posterior medians. Thus are effected the arterial chains. From 
the anterior spinal artery at the bottom of the anterior fissure minute 



THE XOX-XEUROXIC DISEASES 



4 6; 



branches enter and supply the greater part of the central gray matter of 
the cord. They do not supply the posterior horns. From the periphery 
of the cord other branches from the arterial chains dip into the white 
matter and the posterior horns. The artericr sulci come from the an- 
terior tract, pass into the cord and reach the anterior commissure. 
Here as arterial sulco-commissurales they enter the anterior horns 
and supply them and a small area of surrounding white matter. 



FIGURE 95 (B). 



Clark s col. 
Post, column- 




CfarKs Col. 



Ant. Co L 

Eighth DorsaL 



oot 



Tost, 
root 





Ant. root 
First Lumbar. 



Claries col. 




Coajmiss.ce/ls 



Ant root 
"Zaterol eel' 9 

Third Sacral. 
Median cells 

First SacraL 

— Showing Arrangement of Gray and White Matter at Different Levels 
of the Cord (After Merk«l). 



Clarke's column is supplied by branches from these anterior arteries. 
Most of the white matter and the posterior horns are supplied by the 
vasocorona or minute arteries which dip directly into the cord from the 
pia mater. 

The practical points about all these arteries of the cord arc that 
the anterior and peripheral set do not anastomose, that they arc ter- 
minal arteries, that the anterior arc larger than the peripheral and are 
so much larger than the corresponding venous system that their blood 
pressure is probably very high. 



466 



THE NON-NEURONIC DISEASES 



The first sight to catch the eye, after making a transverse section 
of the cord, is the arrangement of the gray and white matter. The 
gray matter is in the center and by means of the cross bar of the 
H-shape connects the two halves of the cord. Outside of the gray 
matter and constituting the edge of the cord spreads the white matter. 
As the ends of the H-like gray matter correspond with the anterior 



FIGURE 96. 

TRANSVER8E 
SECTION OP HALF THE 
SPINAL MARROW IN THE 
LUMBAR - ENLARGEMENT 

(Allen Thomson), f 

This is a seinidiagram- 
matic representation taken 
from a specimen, and 
founded in part on the 
statements of Lockhart 
Clarke and of Kolliker. 

1, anterior median fis- 
sure \ 2, posterior median 
fissure ; 3, central canal 
lined with epithelium ; 4, 
posterior commissure ; 5 % 
anterior commissure ; 6, 
posterior column ; 7, la- 
teral column ; 8, anterior 
column ; 9, fasciculus of 
posterior nerve-root enter- 
ing in one bundle, a part 
of which passes into the 
posterior cornu, and a part 
into the posterior column ; 
10, fasciculi of anterior 
roots ; a, a, caput cornu 
posterioris with the gelati- 
nous substance of Rolando ; 
b, the cervix cornu ; c, pos- 
terior vesicular column of 
Clarke ; t$ the right of d t 
the group of cells in the 
intermedio - lateral tract ; 
r, e, fibres of the anterior roots, entering the anterior cornu, and passing through among 
the cells ; «', fibres from the anterior roots which decussate in the anterior commissure ; 
<", external fibres from the roots running round the outside of the anterior grey cornu 
towards the lateral columns ; /, fibres from the posterior commissure and from the pos- 
terior cornu running towards the anterior. Three groups of cells are seen in the anterior 
cornu in this region of the cord ; and from thfir position may be described as external, 
internal, and posterior. 

(From Quain's Anatomy.) 




and posterior nerve-roots respectively, we see that the white matter 
is naturally divided, as the nerve-roots cross it and enter the gray 
matter, into the anterior, lateral and posterior columns that made up 
the superficial arrangement of the cord. If we make other sections 
of the cord we find that the general appearance remains the same, b'-t 
that the relative amounts of gray and white matter differ at different 
levels. In the cervical and lumbar enlargements we note especially 



THE XOX-XEUROXIC DISEASES 



467 



the relative increase of gray matter ; and high up in the cervical region 
it is beginning to lose its regular H-like outline. 

Beyond a cellular-like appearance in some parts of the gray matter 
and perhaps the greater vascular supply of this over the neighboring 
white matter, the appearance of the central canal in the middle and 
some other unimportant features, we cannot learn much more about 
the cord from a mere macroscopical examination. 

The moment we turn the microscope upon the picture, however, 
and especially if we avail ourselves of the marvelous staining methods 

FIGURE 97. 




Part of the gray matter of the anterior horn, with the neighboring portion of the lateral tract, 
showing the fine medullated fibres which pass from the lateral tract into the gray matter, sur- 
rounded by (pigmented) nerve-cells. (Stained by Weigert- Pal's method.) (After Kolliker.) 

of modern histological research, we are confronted with a most beauti- 
ful and suggestive view. The gray matter is at once seen to be made- 
up of a great mass of neuronic cells with their interlacing proces 
all supported by a matrix of rich neuroglia, connective-tissue and vas- 
cular elements. The cells are variable in size, seem to be specially 
grouped together here and there and send their processes into almost 
every imaginable direction. The processes that run horizontally a< 
the cord will, of course, be seen in their full length like fine hairs. 
Those that run up and down in the cord will, being cut across, appear 
as minute spots with a delicate ring of white matter around them. 
Those that pass here and there obliquely will, of course, present a 
more or less oval appearance with the spot in the middle. 



4 68 



THE NON-NEURONIC DISEASES 



It is clear then that we have in the gray matter of the cord a repre- 
sentative ganglion or bunch of neurone-cell bodies. 

A full description of a neurone will be found in an earlier part of 
the book in a section headed the Neurone and the Neurone Doctrine. 

FIGURE q8. 




Diagram of the Relations op the Cells and Fibers op the Spinal 
Cord. (Baker, after Lenhossek.) 

The right side shows the cells of different classes found in the cord, and their processes. The 
left side gives the processes of cells whose bodies are either beyond the cord or at other levels, 
with the distribution of their collaterals. 

a, a. Motor cells of the anterior horn. 

c. Commissural cells. 

d. Golgi commissural cell. 

e. e. Columnar cells of anterolateral column. 

f. f. Columnar cells of posterior column. 

g. Golgi cell of posterior horn. 

1. Fibers of posterior root forming the ant*ro-posterior reflex, tract. 

2. Fibers passing to the column of, Clarke. 

3. Commissural fibers of posterior root* 

4. Fibers that enter the posterior horn, 
k, k. Collaterals of antero-posterior column. 

1, 1. Collaterals from the pyramidal tracts. 



The cells in the anterior part of the gray matter are larger and 
more angular than they are in the middle or posterior part. Moreover, 
they arrange themselves in little groups that can almost be observed 
with the naked eye. These groups are seen to lie anteriorly and 
antero-laterally and from them run processes that finally pass out 
through the anterior nerve-roots. Another group is seen near the 



THE NON-NEURONIC DISEASES 469 

outer and mid-lateral part of the gray matter. The course of their 
processes is not quite so distinct. In the middie of the gray matter 
just a little back of the end of the cross-bar of the H is another group 
of small cells which make up the column of Clarke. And finally, in 
the posterior parts are scattered groups of quite small and roundish 
cells, intermingled with processes that come in from the posterior 
nerve-roots. 

On account of the gross and minute differences thus observable 
in the gray matter of each half of the spinal cord, it will be convenient 
for us to use the names of the old anatomists and speak of the anterior 
part as the anterior horn, the middle-lateral part as the middle horn, 
and the posterior part as the posterior horn. If we look upon the 
various groups of cells, just described, m their longitudinal distribu- 
tion up and down the whole cord, we may justly speak of them as 
vesicular columns. In the anterior horns, therefore, are two vesicular 
columns, an anterior and a mesial. In the lumbar region there is a 
third or posterior vesicular column of the anterior cornu. Laterally 
between the two horns is the inter -me dio-lateral vesicular column, and 
at the base of the posterior horn, internally, is the posterior or vesicular 
column of Clarke. In the posterior horns the cells are not so well 
grouped as to be contemplated in the light of vesicular columns. 

When we turn the microscope upon the white matter of the cord 
we note a marked change in the appearance of the field. There is a 
complete absence of ganglionic cells and instead a well-packed mass of 
transversely cut fibres. They appear as little rings with a stained 
dot, the axis cylinder, in the middle of them. The position of the dot 
in the ring and the shape of the ring will depend, of course, upon 
whether the fibre happened to be cut transversely or obliquely across. 
These fibres vary in size, the largest of them appearing in the posterior 
part of the lateral columns, and the smallest in the neighborhood of the 
processus reticularis. It is clear that they are the medullated processes 
from some neurone bodies embedded somewhere in the ganglionic sub- 
stance of the cerebro-spinal axis. 

Around the outer edge of the sectional field of the cord we 
notice a layer of neuroglia)- tissue. It sends septa transversely into 
the cord and thus subdivides the white columns into a number of 
smaller columns, which have a relatively fixed position. The neuroglia 
is relatively abundant in a ring that surrounds the central canal. 
Along the line of the posterior roots the peripheral neuroglia enters 
into the posterior horns and there expands to form the substantia 
gelatinosa of Rolando. 

The minute description of the histological elements that we have 
just been observing, including the neurones, the neuroglia and the 
rest of the substentacular tissue, will be found in the chapter headed 
the Neurone and the Neuronic Architecture. 

We have now to analyze further, if possible, these columns and 
vesicular masses of gray matter. The methods that enable us to «!-< 
this are experimental and pathological. The degeneration, r< 
tion and development of the neurone, together with tin- happy dis- 
covery that certain parts of the neurone stain different!) with different 



470 



THE N&N-NEURONIC DISEASES 



clinical reagents, enable us to trace out with an exquisite beauty of 
detail the paths of the various impulses through the cord. This has 
been referred to partly elsewhere. 

The neurone body being the center of nutrition for the entire 
neurone, if it is destroyed the neuraxone immediately begins to break 
down and in a short time is entirely gone. Sometimes we can accom- 

FIGURE 99- 




—Transverse section through half the spinal cord, showing the ganglia : 
A, anterior cornual cells; B, axis-cylinder process of one of these going to posterior 
root; c, anterior (motor) root ; D,, ^posterior (sensory) root; E, spinal ganglion on 
posterior root ; F, sympathetic ganglion ; G, ramus communicans ; H, posterior 
branch of spinal nerve ; 7, anterior branch of spinal nerve ; a, long collaterals from 
posterior root-fibers reaching to anterior horn ; 6, short collaterals passing toClarke's 
column ; c, cell in Clarke's column sending an axis-cylinder (d) process to the direct 
cerebellar tract: e, fiber of the anterior root; /, axis-cylinder from sympathetic 
ganglion cell, dividing into two branches, one to the periphery, the other toward 
the cord ; g, fiber of the anterior root terminating by an arborization in the sympa- 
thetic ganglion ; h, sympathetic fiber passing to periphery (Ramon y Cajal). 



plish this result by direct experiment. More often and better, dis- 
ease accomplishes it for us. It is easy to be seen that if by an ex- 
perimental or pathological insult, a minute focal lesion is established 
in a mass of neuronic gray matter, the processes from the damaged 
neurones can be traced throughout their long course by the degenera- 
tion they undergo. Both primary and secondary neuronic diseases have 
Uvii most invaluable aids to histology and physiology in this way. 

When a neuraxone is cut across artificially or severed from its 
cell-body by a pathological process, that part of the neuraxone that 
has been cut off undergoes complete and rapid degeneration. The 



THE NON-NEURON IC DISEASES 



471 



proximal' part undergoes a much slower and partial degenerative 
process. If a great bundle of neuraxones be thus treated, the appear- 
ance in the variously lengthened severed ends will be that of a de- 
generation that seems to begin at the place of damage and travel 
towards the periphery. This is known as secondary, or Wallerian, 
degeneration, after the man who first called attention to it. The 
degeneration, it is to be again repeated, is always in the direction 
away from the related cell body or center of nutrition. When the 
white matter of the cord is cut across it is noticed that in some parts 
of the columns the degeneration travels upward, in other parts down- 

FIGURE 100. 




A SMALL PORTION OF A TRANSVERSE 8E0TION OF THE HUMAN SPINAL CORD. 

Highly magnified. (B. A. S.) 

a, a, superficial neuroglia ; b, b, transverse section of part of the lateral column of the 
cord in which the dark points are the axis-cylinders, and the clear areas the medullary 
substance of the nerve-fibres : the superficial neuroglia is seen to exhibit the appearance 
of a fine network in which numerous nuclei and one or two corpora amylacea (c. a) are 
embedded, and to extend inwards among the nerve-fibres. 

(From Qnain's Anatomy.) 

ward. Obviously, then, we have to look for the cell-bodies of the 
former below the cut and of the latter above the cut. In this way the 
afferent and efferent tracts of the cord have been most accurately 
traced out and their cellular origin definitely located. 

After a large number of these tracts were thus mapped out and 
demonstrated by experimentation upon the lower animals, and by 
disease in man, it was discovered that they did not all develop simul- 
taneously and to the same degree in the embryo. Some appeared and 
reached maturity earlier than others. The acquisition of the myelin 
sheath was taken as a fair evidence of the full development <>\ a 
neurone and its neuraxone. This process of inclination then not 
occurring at the same time in all tracts of the embryo, it was only 
necessary to get a sufficiently large series of embryos representing dif- 
ferent ages and stages of development, and to study them, in order 
to follow out the lines of location of these particular tracts. Tin's was 
the embryonic method of Flechsicr to which we are indebted for much 



472 THE NON-NEURONIC DISEASES 

of our knowledge of the minute pathways in the nervous system, es- 
pecially in the brain. 

Comparative zoology and embryology, coupled with the observa- 
tions of evolution and biology, have lent their aid and given much 
valuable information. 

Finally, the marvelous staining methods, for which we are hi 
debt to Golgi, Ramon y Cajal, Nissl, Marchi, Van Gehuchten and a 
host of enthusiastic and untiring investigators, have laid bare for us 
the architecture of the very citadel of thought and life. Certain 
reagents, as bichromate of potash, osmic acid and nitrate of silver, 
methylene blue, hematoxylin, when properly used, cause changes of 
coloration in certain parts of the neurones. It would be out of place 
to consider in detail here these various methods, but their great im- 
portance in giving us a proper conception of the structure of the 
nervous system must be acknowledged. It was out of the results of 
the employment of these methods that the neurone doctrine was 
formulated, one of the grandest and most useful scientific generaliza- 
tions ever made in the realm of medicine. 

As a lesult of all these methods of investigation we have learned 
that the white matter of the cord consists of three kinds of tracts, 
projection tracts, commissural and associating. 

The anterior commissure, just at the bottom of the anterior fis- 
sure, transmits neuraxones that run from one side of the cord to the 
other. 

The association or short tracts make up all of the anterior, lateral 
and posterior columns that are not included in the projection tracts. 
They connect one level of gray matter with another and thus, like long 
and short stitches, sew, as it were, the various ganglionic segments of 
the cord together. The parts of the columns where these association 
fibres exist reveal, when cut across, both upward and downward de- 
generation. 

The projection tracts are several in number and need special de- 
scription. Those that connect the brain with the cord are motor in 
function and degenerate downwards. Those that connect the 
peripheral nerves of sense with the cord, and certain parts of the cord 
with the brain, are sensory and degenerate upwards. These tracts 
consist of the following : 

1. Direct or Uncrossed Pyramidal Tract. Turck's Column. This 
is a small tract that lies immediately on either side of the median fis- 
sure. It only extends as far as the middle of the dorsal region. Its 
fibres are the processes of the cells in the Rolandic area of the cerebral 
cortex. They do not change their direction until just before they 
terminate, when thev bend somewhat at a right angle possibly, cross 
to the other side of the cord through the anterior commissure, and 
finally arborize at various levels around the cells in the anterior horns 
of the upper part of the cord. 

2. Indirect or Crossed Pyramidal Tract. This is rather a large 
tract, found in the posterior part of the lateral columns. It nowhere 
approaches the edge of the cord and, except at its postero-internal 
edge, it is separated by the lateral limiting ZO ne from the posterior 



THE XOX-XEUROXIC DISEASES 



473 




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474 



THE NON-NEURON IC DISEASES 



horn. It represents the neuraxones of the cells of the Rolandic cerebral 
cortex. These processes all cross at the decussation of the pyramids, 
pass down the opposite side of the cord and then arborize around the 
cells of the anterior horn at various levels all along the cord. 

FIGURE 103. 




Diagram of the tracts of the cord. 

The crossed and uncrossed pyramidal tracts represent respectively 
ninety and ten per cent, of the entire cerebro-spinal motor paths. In 
spite of the misleading name of the latter, they both carry inhibitory, 
controlling and volitional impulses from one side of the brain respective- 
ly to the opposite vesicular columns of the anterior horn of the cord. 
Speaking from the neuronic standpoint, they constitute the upper 



THE NON-NEUROXIC DISEASES 475 

motor segment. There are no other projection motor paths in the cord 
that we know of. 

3. Poster o-median Tract. Golfs Column. Funiculus gracilis. 
This is a narrow, wedge-shaped tract that lies immediately next to the 
median septum in the posterior column. The point of the wedge does 
not quite reach to the gray matter anteriorly. The column itself does 
not extend much below the mid-dorsal region. It degenerates upwards 
and is thus an afferent or sensory tract. It represents the sensory 
neuraxones that come into the cord by way of the posterior roots of 
the same side and that pass up to arborize around the cells of the 
nucleus gracilis found at the top of the column in the medulla. It 
-carries special forms of sensation from the muscles, the articulations 
-and the tendinous sheaths of the same side. 

4. Postero-lateral Tract. Burdock's Column. Funiculus cunc- 
<itus. This tract constitutes all of the posterior columns, except the 
postero-median columns. It is a very complicated tract and contains 
fibres that degenerate both ways. All afferent neuraxones that enter 
the cord by way of the posterior roots pass sometime through the 
column of Burdach. Some of these fibres have collaterals that bend 
and run downward a short distance in the column, thus simulating 
a downward degeneration. Other fibres of the tract are purely asso- 
ciating, and hence exhibit both an upward and a downward degenera- 
tion. All forms of sensation, tactile, thermic, pain and muscular sense, 
are transmitted by Burdach's column. Some of the posterior root 
fibres that enter it turn around and arborize directly about the cells 
lying in the adjoining posterior horn. Others enter the gray matter 
at the same level, cross through the posterior gray commissure to the 
opposite side of the cord, where they arborize around the cells in the 
opposite posterior horn. Some pass forward into the gray matter and 
arborize around the cells in the anterior horn of the same side. ( Hil- 
ars again enter the gray matter and spread their terminal branches 
around the cells of the vesicular column of Clarke. Still others are 
known to bend upward at a right angle and after giving off a rather 
long descending branch (descending comma trad), continue on their 
way upwards through both Burdach's and Goll's columns, giving off 
collaterals and finally arborizing around the cells that constitute the 
nuclei of the posterior columns (gracilis and cuneatus). 

The column of Burdach is sometimes subdivided into the anterior 
radicular zone, or that part of it which lies next to the posterior horn 
(many association fibres connecting different levels of tin- posterior 
horn with each other run along in this zone) ; the postero-internal radic- 
ular zone; and the lesser radicular cone with its two kinds of fibres. 
That part of the posterior column that is just behind the gra) com- 
missure is sometimes spoken of as the ventricular zone. 

5. Direct Cerebellar Tract. This narrow tract lies along the 
outer edge of the lateral column and extends from the cA^v of tin 
posterior horn around forward to about midway of the column. It 
is a long tract and represents the neuraxones fro n the cells making up 
the vesicular column of Clarke. The fibres enter the cerebellum on 
the same side and arborize around other cells in the cerebellar cortex. 



4/6 THE NON-NEURONIC DISEASES 

The tract degenerates upward and is therefore sensory in function. 
It carries impulses from the muscles, joints and viscera and belongs to 
the indirect sensory system. 

6. Antero-lateral Ascending and Descending Tract. Goiters' 
'Tract. Ventral Cerebrospinal Fasciculus. This tract also lies on the 
edge of the lateral column and extends from the middle o*f the edge, 
where the direct cerebellar tract ends, on around forward as far as, 
and even somewhat to the other side of, the anterior roots. It reaches 
down the side of the lateral column as far as the lumbar region. It 
is supposed to represent the neuraxones of the cells found in the pos- 
terior horns of the opposite side of the cord. These neuraxones pass 
upward and arborize around other cell bodies nesting in the optic 
thalamus. The tract is sensory, as it degenerates upwards. Pain and 
temperature sensations are supposed to be transmitted by it. We are 
in need of further information, however, about the tract. 

Goll's, Burdach's, direct cerebellar and Gowers' tracts are all of 
the projection sensory paths that we know of. Through them pass 
all of the various sensory impulses that have entered by way of the 
posterior roots and are on their way to the sensory cortex of the brain. 

The remaining parts of the columns of the cord are the anterior 
fundamental root zone, embracing the anterior root fibres and including 
the lateral part of the anterior, and anterior p'art of the lateral col- 
umns ; the lateral limiting layer, or mixed lateral zone, along the lat- 
eral edge of the gray matter in the lateral column ; and the zone of 
Tissaucr just at the edge of the posterior horn. We know very little 
about these except that they degenerate both ways and thus contain, 
in all probability, short association tracts. W nether any other sort of 
tracts run through them we do not know. 

In describing the minute anatomy of the spinal cord I referred 
somewhat to some of its more important physiological functions. As 
there are other special functions, it may be well to present here a brief 
resume of all of the activities of this part of the nervous system. I 
shall thus refer to (a) Conduction, (b) Reflex Action, (c) Automatic 
Reflex Action, (d) Vasomotor Action, (e) Trophic Influence, (f) 
Tonic Influence. 

The segmental character of the ganglionic gray matter, as shown 
in the serial arrangement of the spinal nerve roots, is an evidence of its 
primitive structure. Somewhat after the manner of a low articulate, 
such as a worm with its various metameres attached end to end as it 
were and each presided over by a central gray mass with outlying- 
afferent and efferent processes, various levels of the human body are 
presided over by the particular segments of the cord. This is so true 
that we make use of this segmental arrangement and its peripheral 
representation to base many of our spinal localization diagnoses upon. 
Fn spite of the fact that the segmental ganglionic spinal centers are 
welded tightly together by innumerable association tracts, and are 
powerfully dominated by the highly developed anterior segments that 
enter into the morphological structure of the brain, their primitive 
segmental functions are still in marked evidence in the reflex and 
automatic functions of the cord. 



THE XOX-XEUROXIC DISEASES 4J7 

Both in its anatomy and in its physiology we behold in the cord 
the most elementary part and condition of the nervous system. There 
are animals that are devoid of a brain, but there are no animals that 
are without a more or less primitive spinal cord. The functions, the 
essential functions, of the cord, therefore, are of a crude, simplified, 
automatic nature. In a general way they represent a mere form of 
reflex irritability. The central gray deposits constitute the mere center 
through which plays the reflex sensory-motor impulse. 

Whether this sensory-motor impulse has to do with the somatic 
musculature, the blood vessels, the viscera or the genital apparatus, 
it is, after all, but a low-grade automatic function. The trophic and 
tonic control of these outlying tissues by the spinal gray matter is 
largely of a reflex and low order. 

Such are the essential functions of the spinal cord and such is 
the organ in its independently working mass of gray matter with its 
projecting motor processes (anterior root fibres) and receiving sen son- 
processes (particular short posterior root fibres). Were we creatures 
endowed with nothing but a spinal cord, we would lead a low, auto- 
matic sort of a life. Our vegetative organs would go on functionating, 
but our muscles would be in a state of constant tension from the cease- 
less inpouring sensory stimuli. We would be the victims of every 
form of mere reflex stimulation, moving hither and thither, without 
purpose, without reason, merely as a feather blown by the winds of 
our ever-changing reflexes. Alas ! in disease, it is too often seen that 
human beings reach this sad state almost. In certain forms of idiocy 
and cerebral agenesis it is approached. In extensive lesions of the 
cerebrum and of the upper motor segment whereby the control of the 
brain over the cord is greatly withdrawn, how the muscles stiffen 
and contract, and how the reflexes become exaggerated ! What arc 
associated movements and the waxy, athctoid phenomena but the ex- 
pression of liberated spinal cord? Nay, more, who does not recognize 
in those of weakened brain power the yielding to every gratify- 
ing or alarming form of sensation, even to such a degree as to suffer 
a reflex over-action of the bowels, the kidneys, the sexual apparatus. 
even the muscles? 

We must keep closely in mind, then, that reflex action, of a very 
simple primitive order, is the essential function oi the spinal cord. In 
the direct exhibition of reflex action, the projection tracts of the cord 
take no part. It is probable, more than probable, that the association 
tracts take only a secondary part. 

For a pure reflex action there is needed only an afferent fibre, a 
central relay station and an efferent fibre. This completes the arc. It 
is but a little more complicated and highly developed exhibition of 
the primitive irritability that constitutes the inherent functional prop- 
erty of all nervous matter. This simple type of reflex arc is 
primitive that it limits itself in its essentia] manifestation to a single 
level or segment of the cord. The impulse, say from the skin, pas 
up a particular fibre in the sensory nerve, through the p. >sterior 
ganglion, on through the posterior root of the column of Burdach, 
the posterior horn, to the anterior horn of the same side, where it is 



478 THE NON-NEURONIC DISEASES 

transferred to a motor cell and sent on out over its process, through 
the anterior root, along the motor nerve, to stimulate the correspond- 
ing muscle into action. Such is the essential story of every form of 
reflex action. Corresponding sensory and motor areas, as, for instance, 
the skin and muscles of the same leg, are always the subject of it. 
There are reflexes a little more complicated than these, however, and 
illustrate the old physiological laws of Pfiuger in regard to the spread- 
ing of the reflex action. If the sensory excitation is a strong one in 
one limb, the opposite limb will respond. If a still stronger stimulus 
be used, the upper limbs will manifest the action. This, of course, is 
due to the close association between the special segments in the higher 
classes of animals. 

I have already hinted at the fact that the reflex arc, in a normal 
individual, is not a liberated circuit. Just exactly how it is under the 
control of the brain we do not know, but we believe that certain 
reflex-inhibitory processes pass from the cerebral cortex, or rather its 
cells, down through the pyramidal tracts to arborize around the reflex- 
motor cells in the anterior horns. In this way every reflex arc is 
inhibited from above. We are thus saved from being the victims of 
every stimulus that attacks us and that otherwise would keep us in a 
state of everlasting movement and muscular rigidity. 

It is obvious, therefore, that a reflex may be modified by a con- 
siderable number of, and variously localized, lesions. In the first place, 
any injury to the arc itself, upon the motor or sensory side (neuritis), 
or at the center (poliomyelitis), will diminish or abolish it. In deep 
coma it is lost. Any disease that increases the inhibitory force from 
above may diminish it, as is seen in some cases of hysteria. On the 
other hand, how easy it is to comprehend that it may be exaggerated 
by any disease that suppresses the inhibitory force from the brain. 
Hemiplegia and pyramidal degenerations generally are characterized 
by exaggeration of the reflexes. Slight irritation of the posterior roots, 
when the arc is not broken, also increases it, so does strychnine and 
tetanus and the neuroses, and certain diffuse diseases above the arc 
which exalt the excitability of its center. 

There are many forms of reflex that we could probably trace 
out, but in clinical practice the skin, or superficial, and the tendon, or 
deep, reflexes are those we are most interested in. In the former the 
skin is irritated ; in the latter some muscle tendon is tapped. The 
termination of the reflex may be in a gland, a blood vessel or a muscle. 

I have elsewhere described the more common forms of reflex and 
the methods employed in eliciting them. 

Closely related to the reflex is the automatic function of the cord. 
In fact, this function is a form of reflex in which the sympathetic sys- 
tem relieves the brain and makes the management of the reflex appear 
all the more independent and automatic. In the cord are found here 
and there deposits of cells in the gray matter that clearly preside over 
certain actions of the pupil, micturition, defecation, erection in the 
genital apparatus and parturition. 

In the lower cervical and upper dorsal region of the cord, near the 



THE XOX-XEUROXIC DISEASES 



479 



origin of the first dorsal root, is the ciliospinal center, or group of cells 
which regulate automatically the muscle that dilates the pupil and the 

FIGURE 104. 







^[■CaaUXo 



AtfcuU 



1/<aaU 



Diagram to illustrate the mechanism of a spinal reflex and its inhibition from 
above. 

unstriated muscle by whose contraction the palpebral fissure is en- 
larged. Stimulation of this center, or of its path in tin- anterior root 



480 THE NON-NEURONIC DISEASES 

of the first dorsal nerve, causes the pupil and the palpebral fissure both 
to dilate. 

The genital center, for the erection of the penis and ejaculation of 
semen, is in the gray matter from the first to the third sacral segment 
inclusive. It is not close to the ano-vesical center. From the first, 
second and third sacral nerves arise the nervi erigentes ; from the third 
and fourth spring the ischio-cavernous, transverse perineal and bulbo- 
cavernous. The vasomotor phenomena of the penis are under the con- 
trol of the sympathetic. In the fourth and fifth sacral segments are the 
centers for the bladder and rectum, the former being a little the lower 
of the two. 

The mechanism of micturition, like that of defecation, is explained 
partly upon a hypothetical basis. We know that it is a reflex, but in 
regard to the antagonistic action of the various sets of muscles we have 
little information that is at all positive. In micturition a sensory im- 
pulse is first started from the mucous membrane of the bladder; this 
travels along the second, third and fourth sacral nerves to the spinal 
center and also to the brain. From the spinal center a motor impulse 
passes out through the anterior roots of the third and fourth sacral 
nerves to the common pudendal nerve, or to the hemorrhoidalis medius, 
and so on through the sympathetic to the muscles of the bladder. The 
detrusor muscle and the sphincter vesicae are presumed to act an- 
tagonistically, so that a stimulation of one causes an inhibition of the 
other. When there is a desire to void the urine, the will relaxes the 
sphincter and checks its reflex contraction, while the detrusor, stimu- 
lated from the cord, contracts the walls of the bladder. The act is 
also assisted by the will through the associated contraction of the 
abdominal muscles. The impulses from the brain to the vesical cord 
center are believed by some to travel by way of the antero-lateral tracts. 
It is obvious how disease can disturb the function. Disease of the 
cord above the sacral segment may result in both sensory and motor 
paralysis of a volitional character. The motor reflex, however, may 
not be disturbed ; in fact, may be highly exaggerated. Under such 
conditions there is no desire felt by the patient to void his urine, 
but as soon as the bladder is distended there is a reflex evacuation. 
This is intermittent incontinence of urine. In disease of the spinal 
centers themselves, both sphincter and detrusor are paralyzed and 
there is constant dribbling. The simple elasticity of the mouth of 
the bladder may check this somewhat, by keeping it closed. A total 
section of the cord at any height seems to result in the paralysis of 
the function of vesical and rectal evacuation. This may be but another 
phase of Bastian's phenomenon observed in connection with other 
forms of reflex action. According to Bastian, complete transverse 
lesions of the cord produce loss of all the reflexes below the lesion ; 
where there is exaggeration of the reflex from a transverse lesion, the 
latter is not a complete one. Ischuria, or retention of the urine, results 
from detrusor paralysis. The same result may occur from spasm 
of the sphincter. Ischuria paradoxa is where there is an enormous 
distention of the bladder from paralysis of the detrusor and the urine 
merely drips away mechanically. 



THE JS'OX-XEURONIC DISEASES 48 1 

The same sort of mechanism is supposed to regulate the evacua- 
tion of the rectum. Disease above the center may, as in the case of 
the bladder, shut off the transmission of both the sensory and volitional 
impulses. In such cases the finger inserted into the rectum will detect 
the vigorous, reflex contraction of the sphincters. The reflex may be 
destroyed in accordance with Bastians hypothesis. 

Other automatic reflex centers that exist in the cord, though we 
know very little about them, are a respiratory center, subsidiary and 
minor to the respiratory center in the medulla, cardio-accelerator cen- 
ter, vasomotor and sudorific centers. 

We can hardly speak of a musculo-lonic center, for though it is 
one of the functions of the cord to keep all the muscles of the body 
in a state of slight tonic contraction, it is a function that probably 
belongs to all of the cells that send out motor impulses. The same 
may be said of the trophic function of the -cells in the anterior horns. 
It is easy to understand how the muscles directly under the control of 
these cells, where the nutritive center for the related neurones has its 
seat, may have their nutrition maintained from the same source. It is 
impossible to say, however, how or from what particular cells the in- 
fluence originates that supports the nutrition of the joints, bones and 
skin. 

Thus far I have described briefly all of the essential functions of 
the spinal cord, and in their final analysis they were all seen to be 
nothing but a simple, low form of sensory motor reflex. Were we 
possessed of nothing but a spinal cord, we would be nothing but auto- 
matic reflex creatures, living and moving in accordance with every 
stimulus that happened to come down upon us. Such is the way that 
such creatures as the amphioxus lanceolatus, with practically only a 
spinal cord, lives in the mud at the bottom of the streams. 

From time immemorial authors have spoken of conduction as one 
of the functions of the cord, meaning by this that through the cord 
passed the impulses, motor and sensory, between the bran: arid the 
body. Such a conception is erroneous and misleading. Moreover, 
it stands in the way of understanding many of the phenomena of 
disease. The cord is not a direct transmitter of impulses, as physiology 
•clearly teaches every day. It is singular how the statement is con- 
stantly repeated in the modern books upon the functions of the nervous 
system, that the spinal cord transmits impulses between the brain and 
the skin and muscles; and yet on the very next page it is demonstrated 
that all impulses, whether afferent or efferent, are first lodged in the 
gray matter of the cord, undergo certain modifications there, and are 
then sent out as distinct original cord impulses. This is a most im- 
portant distinction. It gives the cord the dignity it should hold and 
it explains many of the motor, sensory, reflex and trophic phenomena 
of disease states in a way that cannot even be conceived of upon tin- 
basis of the cord being a mere conduit through which rush the stimuli 
between the brain and the outlying organism. Strictly speaking, 
therefore, conduction is not a spinal cord function, as the function 
has heretofore been usually thought of, and for that reason T 1 
postponed its consideration until the last. 



482 THE NO N- NEURONIC DISEASES 

Let it be clearly understood then that no impulse of any sort, 
between the brain and the periphery, passes without being broken and 
modified more or less in the ganglionic gray matter of the cord. 

The white conducting tracts, which we studied a few paragraphs 
back, are, strictly speaking, not a part of the cord. They are processes 
reaching down from the brain cells above and from the peripheral 
ganglionic sensory neurones from below, to carry the impulses from 
either hand into the gray ganglionic masses of the cord. This was 
clearly pointed out in our discussion of the neuronic architecture of 
the nervous system and in the consideration of the minute anatomy of 
the part of the nervous system called by the anatomists the spinal cord. 

The motor pyramidal tracts are cerebral structures and are loosely 
spoken of as being parts of the spinal cord merely because they lie 
close to it. The same is to be said of the long, projection sensory 
tracts. To emphasize this, which I regard as a most important neu- 
rological fact, let me make use of a homely illustration by saying that 
if a boy in search of jam has his whole arm thrust down deep into 
a long, narrow jar, his arm does not thereby become a part of the jar 
or be regarded as entering into the general functions of the jar. In 
the same way the cortical neurone cells, thrust their long arms down 
along side of the true spinal cord, consisting of its various segments of 
gray deposit bound together by short, associative tracts of white mat- 
ter, and with their arborization fingers, so to speak, stimulate, inhibit 
and control the cells in the cord that stimulate the muscles and sub- 
serve the movements of the body. Here again we observe the beau- 
tiful uniformity and consistency of nature. Such a phenomenon is 
again nothing but a reflex, but the stimulus comes from the brain this 
time and not from the skin or tendon. The movement that is pro- 
voked by it is said to be a volitional, a sort of intellectual movement, 
because the afferent stimulus to the cord comes from a finer and more 
complicated source, the cerebral mechanism and cells that underlie 
psychic acts, but the movements of the muscles themselves are imme- 
diately due to the cord stimulation and are the result of the old, 
primitive reflex function of the spinal cord. 

The whole phenomenon then of a volitional impulse is of the 
nature of a higher form of reflex, so far as the spinal cord is con- 
cerned. 

It would probably take us wide of the mark to discuss here 
whether the impulse that starts from the cerebral cortex, and which 
eventuates in a so-called volitional movement, originates there or is 
itself a reflex acting under the stimulus of an impulse sent up from the 
skin by way of the spinal cord. The question is a philosophical one 
and belongs to psychology. Nevertheless it must be noted here that 
very often such so-called volitional impulses are the direct result of 
fresh afferent stimuli. This is a matter of daily common observation. 
These afferent stimuli do not reach the brain cortex in the original 
state in which they started from the periphery. Our anatomy shows, 
and physiology and pathology amply prove, that they are first received 
from the peripheral sensory neurones into the gray ganglionic deposits 



\ 



THE NON-NEURON1C DISEASES 483 

of the cord, are there switched off and in all probability modified, and 
then sent on up as cord impulses to the brain. In other words, our 
cortex, our consciousness, does not anywhere directly perceive the 
original stimulus that affects the outermost organ of sense ; it only 
perceives the related stimulus from the cord. It is a startling fact, 
but one none the less true, that our real sensations are from the cord. 
We have no conception of what the skin feels, except as the cord in- 
terprets it to us. How obvious this is sometimes. Take the following 
illustration: A man touches a red hot plate. Two phenomena take 
place from the one instantaneous stimulation. The first is the simple 
cord reflex without the sense of pain. The hand is jerked away before 
the man realizes it. The second is the feeling of pain which comes a 
second or two after. Was the stimulus changed ? No, but the cord 
perceived the stimulus and acted accordingly (reflex) ; the brain ex- 
perienced the cord's commotion and in the language of the brain called 
it pain. The significance of this from the clinical standpoint is of 
tremendous importance. It clarifies the discussion in regard to the 
nature of pain. It shows how it is really a cerebral (mental) phenome- 
non, though dependent upon the physical basis of the cord and its 
condition. It will lead to the avoidance of such childish conceptions as 
that pain is located in the skin somehow, or in the peripheral ends of 
the nerves, and that there is no such thing as pain without some gross 
lesion that you can cut away with the knife. It opens the way for 
the clearer conception of psychalgia and mental pain, such as are some 
of the pains of hysteria. Moreover, it accounts in part for our greater 
ignorance of the spinal pathways for the various forms of sensation, 
as compared with our knowledge of the motor pathways. An efferent 
impulse always terminates in the same sort of an element, which in 
its last analysis, whether it be muscular, glandular or vasomotor, is 
largely a contractile or muscle-like element. Afferent impulses may 
terminate in a number of different sorts of cellular combinations and 
elements in the cord. These travel up in various ways toward the 
brain, which puts its own interpretation upon them, calling some touch, 
some heat and some pain. Of course, the nature of the end apparatus 
which first receives the stimulus determines the pathway along which 
it shall travel, and thus the brain interprets it. This is glaringly dem- 
onstrated in connection with the special senses. Vibrations doubtless 
hit all organs and parts of the body alike, but the eve directs the one 
set along the optic nerve and the brain calls the vibratory movement 
light, the ear directs another set along the auditory nerve and the brain 
calls it sound. Both sets of vibrations, however, are interrupted and 
doubtless prepared for the brain by the optic centers in the corpora 
qnadrigemina, etc., and by the auditory nucleus in the medulla. It is 
not the eye or the ear that the brain itself perceives, bul tin- commo- 
tion in the primary optic and auditory nuclei. 

The functions of the motor and sensory projection tracts ma 
recapitulated as follows : 

Crossed and Uncrossed Motor Tracts. These hear impuls 
chiefly of an inhibitory and controlling character, from the cerebral 



484 THE NON-NEURONIC DISEASES 

cortex to the motor ceils of the anterior horns of the cord. If they are 
diseased so that they excite the cord cells, spasmodic movements may 
occur in the limbs and body, involving groups of muscles that sub- 
serve volitional, purposive, intellectual physiological acts. Individual 
muscles are not thrown into a state of spasm. In the higher cerebral 
and psycho-neurotic disorders, like hysteria, permanent spasms and 
contractures may be produced. Note always, however, that the whole 
limb, or part of the body, is affected in an attitudinizing manner, and 
not distinct muscles. The reflexes and even the normal automatic 
functions of the cord may be thus stimulated and exaggerated. When 
the disease of these motor tracts is such as to suppress their control 
over the anterior horn cells, paralysis of a spastic character occurs in 
the limbs. The reflexes are exaggerated. Here again physiologically 
associated muscles and groups of muscles are affected, not individual 
muscles. There is no atrophy and the electrical reactions are un- 
changed. Spastic paraplegia and exaggeration of the reflexes are the 
principal manifestations of disease in these tracts. These are usually 
bilateral. Other symptoms as well as these will be considered under 
the head of diseases of the brain. 

Postero-median Tract. GolVs Column. This tract carries special 
sensations from the muscles, articulations and tendon sheaths of the 
same side to the cells of the nucleus gracilis in the medulla. When 
it is diseased the muscular sense, including the position of the limbs 
and the power of estimating weights, is lost. Incoordination of move- 
ment, or ataxia, occurs, and probably some astereognosis. 

Postero-lateral Tract. Burdach's Column. All forms of sensation 
pass through this compound and complex bundle of afferent processes. 
When it is diseased, all forms of sensation are disturbed ; ataxia oc- 
curs ; astereognosis, loss of the reflexes and every physiological act 
that involves sensation, directly or reilexly, are diminished or abol- 
ished. 

Direct Cerebellar Tracts. As these carry sensations to the cere- 
bellum, their disease results in a loss of equilibrium. 

Ant cro -lateral Tracts. Gowers' Tracts. Through these pass the 
pain and temperature sensations that originate on the opposite side. 

It is to be understood, as I have tried to show, that, like the optic 
and auditory tracts, these tracts that seem to carry special cutaneous 
sensations, do so merely by reason of the adaptability of their end 
organs to receive particular sorts of vibrations. Just as the cortex does 
not directly see and hear the outer world, but merely interprets into 
the psychic terms of light and sound, the commotion produced in the 
primary optic and auditory nuclei, so it does not feel the outer world 
directly pressing against the skin, but merely interprets into the 
psychic terms of touch and heat and pain the commotion produced 
in the spinal and other nuclei where the processes of these so-called 
spinal sensory columns terminate and arborize, or possibly in some 
higher ganglionic center like the optic thalamus where the next set 
of afferent neurones terminate. Our knowledge of the sensory func- 
tions is not as well defined as could be desired. 



THE NON-NEURONIC DISEASES 485 

SPIXAL LOCALIZATION AXD TOPOGRAPHY. 

The topography and localization of lesions within the spinal cord 
are important from the standpoint of surgery. The segmental charac- 
ter of the cord arrangement here serves us well. At regular intervals 
emerge from the cord the anterior and posterior roots which unite 
together to form mixed nerves that issue from the spinal canal by way 
of the intervertebral foramina. High up in the cord the foramina are 
nearly opposite the place of emergence of the spinal roots. As the 
cord is shorter than the vertebral column, it necessarily follow c mat 
the lower we go down the cord the lower the foramina will be in rela- 
tion to the points of emergence of the roots. The latte: are thus 
oblique and are obliged to run a more and more descending course, 
after they leave the cord, to reach the vertebral outlet. It becomes a 
matter of the first importance, therefore, to comprehend the topo- 
graphical relationship of the vertebra to the underlying segments of 
the cord. The spinous process of each vertebra is selected as the 
point beneath which it is desired to know what particular segment of 
the cord may be lying. This has been carefully worked out and the 
accompanying diagram of Cowers' reveals the facts in a most graphic 
way. It will be noted that except in the cervical region, and even 
here to some extent, the segments of the cord are to be respectively 
found two and three spines higher than the spine of the same number. 
For instance, the seventh spinal segment is directly beneath the fifth 
vertebral spine. In the cervical region the segment is only one remove 
above the corresponding vertebra. According to Reid and Starr, there 
are marked individual differences in regard to the topographical rela- 
tionship between the vertebrae and spinal segments. 

The determination of the segmental localizations involves a knowl- 
edge of the functions of the nerve roots. It is needless to say that 
the anterior root is efferent and carries motor and trophic impulses 
from the cells of the anterior horns to the muscles of the body. Nor 
need it be repeated that the posterior root is afferent and brings in 
sensory impulses from the skin and other sensory organs. If, there- 
fore, we can work out the correspondence between the segmental 
origin of these nerve-roots and the particular muscles and 
cutaneous areas that their composite nerves innervate, we 
will have a definite guide in the distribution of the atrophic 
paralysis and the amesthesia to the exact segmental seat of 
the lesion. Allowance must be made somewhat for the fact that no 
segment is absolutely alone in its action, for it is associated in func- 
tion with the neighboring segments, and thai no motor or sensory root 
is limited absolutely to one segment for iis internal origin. 

A segmental lesion does not produce 1 a complete muscular atrophy, 
for instance, because the adjoining unaffected segments assist to 
maintain the muscle's nutrition. The same is true in regard t<> the 
sensation. A lesion of a single pair of posterior nerve roots maj not 
even be noticed on account of sensory disturbance; and a small lesion 
in a particular segment may not cause any anaesthesia in the area of 
distribution of the corresponding nerve. 



4<SC> 



THE NON-NEURONIC DISEASES 



FIGURE 105. 

MOTOR. 



St.-Mastoid 
Trapezius 

Diaphragm 




SENSORY. 

Neck and scalp 
Neck and shoulder 

Shoulder 

Arm 

Hand 



Front of thorax 
Ensiform area 



Abdomen 
y (Umbilicus 10th) 



r Buttock, upper 
\ part 

I Groin and scrotum 
"i front 

f outer side 



ThiRh 



front 



inner side 



Leg, inner side 
f Buttock, lower 
part 



Back of Thigh 
Leg 
and 
Foot 



r except 
1 inner pan 



Perinaeum and Am 



from coccv; 

nub 



REFLEX. 



Scapular 



Epigastric 



Abdominal 



Cremasteric 
\ Knee rejiex 



Gluteal 



Foot clonus 
Plantar 



A Diagram Designed to Show thb Relations op the Vertebrae to the 
Spinal Segments, and of the Spinal Nerves to the Motor, Sensory, and Reflex 
Functions of the Spinal Cord. (Gowkrs ) 



THE XOX-XEUROXIC DISEASES 



487 



For our knowledge of these segmental and peripheral correspond- 
ences we are indebted to Starr, Mills, Ross, Thorburn, Sherrington, 
Bruns, Sachs and others. Following their teachings, I will give the 
muscles, areas of sensation and the reflexes, and the corresponding 

FIGURE 106. 



LOCATION OF THE SEGMENT 

FOR 



Sensibility. 



Motility. 



Smell 



Thalajyn Muscles 



Sight 

Head 
Eyes 
Face 

Tongue I 

s 3 

'Hearing \ £ 

Pharynx J * 

Larynx 

(Esophagus 

Viscera of 

Chest and Abdomen 

Occiput. 



Shoulder 
g> C Musculo spiral nerve 

i 



Median nerve. 
& I Ulnar nerve ... 



II 



Pulv 



.Sphincter of the iris 

ciliary 

-Internal rectus, levator palpebrtt- 
rectus, inferior and superior 
'Inferior oblique 
.Superior oblique 
Masseter, temporal, 

pterygoids [(upper facial) 

External rectus, frontalis, orbicularis of 

Mimetic face muscles (lower facial) 
Mouth and throat muscles 
Laryngeal muscles 
Tongue muscles 
Sterno-cleido mastoid 
Deep neck muscles 

Trapezius, Serratus anticus 

Diaphragm 

Deltoid, Diceps, pectoralis (clavicular part) 



rachialis anticus, supinator longus 
triceps, latissimus dorsi, pectoralis (cos 
Extensors of the h' ngers and phalanges j 






Flexors of the fingers and phalanges 
Interossei and lumbricales , 
Thenar, hypothenar \ 



Fore- 
arm. 



Thorax 

Epigastrium 



Gluteal reglou 
Inguinal region 



Thigh 



Leg 



Hip 
anterior 

external 

posterior 

internal 

anterior 

Foot 

rotuin, Penis, etc. 

Rectum, Bladder 



Intercostal muscles 
Back muscles 
AlKloniin.il muscles 



— _ Ueopsoas 

Snrtoriiis 

...... Adductors 

Abductors 

Quadriceps ' 

Flexors 

Extensors 



Thigh 



Leg 



r„nrl 

, xtensors of foot and boaa 

rthMtl __, 

rlneal ) 
Bladder V Musculature 
Rectum ) 



(After Jakob.) 



segments from which they arc innervated. The accompanying e* 
quisite diagrams of Head will assist in showing the segmental sensory 
innervations. It is to be remembered, however, that there arc no 
sharp lines in nature between the various areas as the picture indie 

Ope area blends into its neighbors, hence the sensor) localizations 



488 THE NON-NEURONIC DISEASES 

must be made guardedly. The reflex and muscular localization mani- 
festations are somewhat more distinctly defined. 

Second and Third Cervical Segments. The sterno-mastoid, 
trapezius, scaleni and deep neck muscles, together with the diaphragm, 
are innervated from these segments. Sensation is perceived through 
them in the back of the head up to the vertex, and in the neck. The 
sensory nerves involved are the occipitalis major and minor, auricularis 
magnus, superficialis colli and the supraclavicular. The so-called 
hypochrondrium reflex is possibly dependent upon them. This con- 
sists of a sudden inspiration produced by a quick pressure beneath the 
lower border of the ribs. This is not an important reflex. It is prob- 
ably due to diaphragmatic excitability. 

Fourth Cervical Segment. The diaphragm, deltoid, biceps, coraco- 
brachialis, supinator longus, rhomboid, supra- and infra-spinatus are 
all partially innervated from this area. The . sensory distribution in- 
cludes the neck, anterior surface of the shoulder and outer surface of 
the arm ; and the following nerves, supra-clavicular, circumflex and 
musculo-cutaneous externally. An important reflex is the pupillary, 
involving the fourth cervical to the second dorsal segments, and re- 
vealed in a dilatation by irritation of the neck. 

Fifth Cervical Segment. This takes part in the innervation of 
many muscles, especially those of the arm. They are the deltoid, 
biceps, coraco-brachialis, brachialis anticus, supinator longus, supinator 
brevis, deep muscles of the shoulder blade, rhomboid, teres minor, 
clavicular portion of the pectoralis and the serratus magnus. The 
sensory area includes the back of the shoulder and arm and the outer 
side of the arm and forearm to the wrist. The nerves concerned are 
the supra-clavicular, circumflex, external and internal cutaneous and 
posterior spinal branches. The scapular reflex, or contraction of the 
scapular muscles by irritation of the skin over the scapula, implicates 
the fifth cervical to the first dorsal segments. The supinator longus 
reflex is the flexion of the forearm by the tapping of the tendon of 
this muscle. 

Sixth Cervical Segment. Here again a large number of muscles 
are innervated — namely, the biceps, brachialis anticus, subscapular, 
clavicular pectoralis, serratus magnus, triceps, extensors of the wrist 
and fingers and pronators. The sensory areas are the outer side and 
front of the forearm, the back of the hand along the radial distribu- 
tion. The nerves chiefly concerned are the external cutaneous, internal 
cutaneous and radial. In the fifth to the sixth cervical segments we 
find the center for the triceps reflex. If the tendon just above the 
elbow be tapped, the forearm jerks in extension. The sixth to the 
eighth cervical contain the center for the posterior wrist reflex, ex- 
tention of the hand occurring when the tendons are struck. 

Seventh Cervical Segment. Here we find the innervation of the 
long head of the triceps, the extensors of the wrist and fingers, the 
pronators of the wrist and its flexors, the subscapular, the costal part 
<>! the pectoralis, the serratus magnus, latissimus dorsi and teres major. 
The sensory innervation includes the radial distribution in the hand, 
the median distribution in the palm, thumb, index and halt the middle 



THE NON-NEURONIC DISEASES 489 

finger. The nerves involved are the external cutaneous, internal 
cutaneous, radial, median and posterior spinal branches. 

The anterior wrist reflex depends upon the seventh to the eighth 
cervical, the wrist undergoing flexion when its anterior tendons are 
tapped. The seventh cervical to the first dorsal contain the centers 
for the palmar reflex. The fingers close when the palm is stroked. 

Eighth Cervical Segment. Here are found the origin of stimula- 
tion for the long head of the triceps, the flexors of the wrist and fin- 
gers and the intrinsic muscles of the hand. It receives sensation from 
the ulnar area of the hand, back and palm and the inner border of the 
forearm. The nerves that preside over this are the internal cutaneous 
and ulnar. 

First Dorsal Segment. This innervates the extensors of the 
thumb, the intrinsic hand muscles and the thenar and hypothenar mus- 
cles. The nerves involved are chiefly the internal cutaneous and nerve 
of Wrisberg, or lesser internal cutaneous. The skin chiefly of the 
inner side of the forearm and arm up to almost the axilla is the sensory 
area involved. 

Second Dorsal Segment. Sensation is supplied through this in 
the inner side of the arm near and in the axilla and the nerve impli- 
cated is the intercosto-humeral. 

Second to the Twelfth Dorsal Segments. These stimulate the 
muscles of the back and abdomen and the erectores spins. They pre- 
side over the sensation of the skin of the chest and abdomen, in bands 
running around the body and downward. These bands correspond to 
the spinal nerves. As I have said, the lines between them are not sharp. 
The sensation from the upper gluteal region is also marked by these 
segments. The nerves that are concerned are the intercostals and dorsal 
posterior nerves. Two reflexes of importance are here represented. 
The epigastric, involving the fourth to the seventh dorsal segments, 
is the retraction of the epigastrium by the tickling of the mammary 
region; the abdominal, involving the seventh to the eleventh dorsal, 
is the retraction of the abdomen, produced by the stroking of its sides. 

First Lumbar Segment. The muscles concerned are the ilio-psoas, 
the rectus and the sartorius. The innervation of the skin involves 
that over the groin and in front of the scrotum. The nerves are the 
ilio-hypogastric and ilio-inguinal. The cremasteric reflex, under the 
control of the first to the third lumbar segments, is revealed in the 
retraction of the scrotum by the stroking of the inner side <»t" the thigh. 

Second Lumbar Segment. The muscles here stimulated are the 
ilio-psoas, sartorius and quadriceps femoris. The skin on the outer 
side of the thigh, by way of the genito-crural and external cutaiM 
nerves, is here innervated. That most important of ail reflexes, the 
patella, in which the knee jerks as the result of a tap on the patella 
tendon, is here represented. 

Third Lumbar Segment. Tin- muscles that receive their n 
supply thence are the quadriceps femoris, anterior part of the bic 
inner rotators of the thigh and the abductors of the thigh. The skin 
area affected is the front of the thigh. The nerves are the middle 
cutaneous, internal cutaneous, long saphenous and the obturator. 



490 



THE XOX-XEUROXIC DISEASES 



FIGURE 107. 




VIII 



Sensory arras of the skin and their segmental representation in the spinal 
cord. (After Head.) 



THE NON-NEURONIC DISEASES 



491 



FIGURE 108. 



C VII 




Sensory areas of the skin and their segmental representation in the spinal 

cord. (After Head. ) 



492 THE NON-NEURONIC DISEASES 

Fourth Lumbar Segment. Here the muscles represented are the- 
abductors of the thigh, the adductors, the flexors of the knee, the 
tibialis anticus and the peroneus longus. Sensation is received from 
the inner side of the thigh, leg and foot; and the nerves involved are 
the internal cutaneous, long saphenous and the obturator. The gluteal 
is an important reflex represented here, though the fifth lumbar seg- 
ment also is involved. Stroking the buttock causes a dimpling in its 
fold. 

Fifth Lumbar Segment. Here we find the source of the nerve 
supply of the outward rotators, the flexors of the knee and of the ankle,, 
the peronei and the extensors of the toes. This segment is in corre- 
spondence with the back and outer side of the leg and ankle, the sole 
of the foot and the dorsum. The nerves implicated are the external 
popliteal, external saphenous, musculo-cutaneous and plantar. 

The Achilles-tendon reflex, another most important reflex, is here 
centralized. A tap on the tendon causes the foot to extend on the calf. 

First and Second Sacral Segments. The muscles represented 
here are the flexors of the ankle, extensors of the ankle, long flexor 
of the toes and intrinsic muscles of the foot. The back and outer side 
of the leg and ankle, the sole of the foot and the dorsum are sensitized 
from these segments. The nerves involved are the external popliteal,, 
external saphenous, musculo-cutaneous and plantar. From the fifth 
lumbar to the second sacral segments is the center for the plantar 
reflex. When the sole of the foot is tickled the toes are all flexed and 
the leg is retracted. 

Third, Fourth and Fifth Sacral Segments. These represent the 
perineal muscles and the muscles of the bladder, rectum and external 
genitals. Here are also located the automatic reflex vesical and anal 
centers ; also the genital and parturition centers. From these same 
segments the skin of the back of the thigh, the anus, the perineum and 
external genitals is innervated. The nerves involved are the small 
sciatic, pudic, inferior hemorrhoidal and inferior pudendal. 

Fifth Sacral and Coccygeal Segments. From hence the coccygeus 
muscle is supplied and the skin about the anus and coccyx. The nerve 
is the coccygeal. 

Symptoms of a Unilateral Lesion. Brown-Scquard's Syndrome^ 
As this is a localization manifestation, it may well be referred to here. 
Brown-Sequard long ago noted that whenever a lesion severs the cord 
half way across, there is complete motor paralysis on the same side 
as the lesion, incomplete sensory paralysis, or anaesthesia on the oppo- 
site side. The reason for this is obvious, as the motor tracts decussate 
in the pyramids above the lesion and the sensory tracts, immediately 
after they enter the cord, below the lesion. Some additional phenom- 
ena, however, accompany the syndrome. The sensory disturbance on 
the side opposite the lesion is an incomplete one because the muscular 
sense is unaffected. The muscular sense on the side of the lesion is 
diminished or lost. The paralyzed side, moreover, is by per. esthetic. 
hyperalgesic and exhibits a slight elevation of temperature. The re- 
flexes on this side are exaggerated ; though at first they may be absent,, 
possibly in accordance with Bastian's hypothesis. If mobility returns 



THE NON-NEURONIC DISEASES 



493 



FIGURE 109. 




Diagram to illustrate Brown- Sequard's syndrome. Modified from Brissaud. 



494 THE NON-NEURONIC DISEASES 

to this side, ataxia, according to Botazzi, Herbold, Oppenheim, sets in. 
On the anaesthetic side, all forms of sensation are lost, except that of 
the muscular sense. Just above the anaesthetic area on the side oppo- 
site the lesion there is a hyperaesthetic zone, just in an area on the 
same side of the lesion and corresponding with the same root-zone 
there is a semi-girdle ring of pain, hyperaesthesia or anaesthesia. 

The accompanying diagram, modified from Brissaud, exhibits in. 
a schematic way the mechanism of Brown-Sequard's syndrome. Dorsal 
stab wounds are the most common cause of it, though it may occur in 
tumors, hemorrhages, syphilitic, sclerotic and even myelitic processes 
that involve the cord half way transversely. The future of these 
unilateral lesions is usually a good one. The symptoms largely disap- 
pear, though rarely completely so. 

Lumbar Puncture. As a means of diagnosis, and in some in- 
stances, perhaps, of treatment, lumbar puncture has become an estab- 
lished procedure. At the beginning of the consideration of spinal cord 
diseases would seem to be the proper place to consider it. Quincke 
first suggested the operation in 1891 in a paper entitled Hydrocephalus 
presented to the Tenth Congress of Internal Medicine. Two years 
later Von Ziemssen reported his experience with it in reducing brain 
pressure. It was Lichtheim who, about the same time, called attention 
to the value of it as a diagnostic procedure. Then followed Furbringer, 
Jacoby and many others, until now it is a familiar manoeuvre. 

An ordinary syringe with a hollow needle is employed. In insert- 
ing it the needle may be used alone or attached to the barrel of the 
syringe. Too short a needle ought never to be used, as ofttimes the 
insertion has to be made to a considerable depth. Sometimes a thick 
needle with a stylet is most desirable. Jacoby used a firm, smooth 
aspirating needle of a millimetre to a millimetre and a half in diameter 
and eight centimetres in length. 

Of course, strict asepsis and sterilization are to be employed, and 
in restless patients an anaesthetic may have to be administered. 

The column should be rendered convex by the patient flexing his 
body forward while sitting or lying, as Quincke recommended, upon 
his left side. The puncture is to be made between the third and 
fourth, or fourth and fifth, lumbar vertebrae, in the middle line in 
children, about one centimetre laterally from it in adults, at the height 
of the lower border of the spinous process, or at about its lower third. 
The needle is made to pierce the skin and then gently inserted upward 
and towards the middle line, until there is no further resistance. Usu- 
ally the needle has to be pushed to a depth of from two to eight centi- 
metres. As soon as the subarachnoid cavity has been entered, the 
ccrebro-spinal fluid begins to appear drop by drop or as a slight stream. 
The latter is due to pressure which may be measured by attaching the 
needle to a manometer. In adults the normal pressure is about one 
hundred and fifty millimetres. Tt varies, however, from one hundred 
and fifty to six hundred and eighty. Quincke found it to vary in chil- 
dren from seventy to four hundred and seventy millimetres. The 
flow, when it has slowed down, rarely exeeeds four drops in a minute. 

Inspiration and expiration modify the flow. Raising the head 



THE NON-NEURONIC DISEASES 495 

increases it. Sometimes a slight change in the position of the needle 
will cause a flow that has ceased to start up. 

There is no absolute rule about the amount of fluid to be with- 
drawn. The object being two-fold — namely, to reduce pressure and to 
secure fluid for examination — circumstances must determine the 
amount. Furbringer has taken off at one sitting one hundred and ten 
cubic centimetres. 

There is very little pain experienced, if aspiration is not resorted 
to. Headache sometimes occurs. Aspiration almost always produces 
pain, sometimes pain that is intolerable. Rarely do any accidents occur 
during the puncture, if care be exercised. The operation, however, 
should not become a routine one, for it is not entirely devoid of dan- 
ger. For instance, a local meningitis may be transformed into a gen- 
eral meningitis by it. A root of the cauda may be pierced and corre- 
sponding pain and neuritis set up. In cases of tumor, aneurism and 
meningitis even, death has followed early the operation. A vein may 
be entered and the needle become clogged. Blood must be avoided, 
as it impairs the diagnostic value of the fluid. 

The needle should be withdrawn while the fluid is still running. 
In this way the entrance of air is prevented. Sometimes considerable 
effort is required in pulling out the needle. This is merely on account 
of the pressure upon the needle of the crossed fibrillar of the fascia. 

The after treatment of the wound is simple and consists of the 
application of a little iodoform collodion and a cotton compress, held 
in place by a piece of adhesive strip. The patient should remain quiet 
in a horizontal position for several hours afterwards. 

As a therapeutic measure, lumbar puncture is of little value. It 
may be employed as a palliative by reducing intra-cerebro-spinal pres- 
sure. Some day it may prove useful for the direct medication of the 
brain and cord. 

As a means of confirming a diagnosis, under some circumstances, 
it is available. Even here, however, it has its limitations. The state of 
the fluid does not always and absolutely indicate the pathological condi- 
tion present. For instance, there may be an inflammatory separation 
of the cranial and spinal cavities and the fluid that is drawn off be per- 
fectly normal, though the cerebral meninges are in a high state of 
disease. The thickened, gelatinous condition of the fluid, sometimes 
observed, impairs the value of the criteria. 

Normal cerebrospinal fluid is colorless and alkaline, and con- 
tains sodium chloride and other inorganic salts. There are o.i per 
cent, of proteids, consisting chiefly of proto-albumose with some 
serum-globulin and rarely peptone. It docs not contain any serum- 
albumin, fibrinogen or nucleoproteid. There is a non-nitrogenous re- 
ducing substance in it which Claude Bernard thought was sugar, but 
which Halliburton regards as pyrocatechin derived from the proteids. 

Pathologically we note in the fluid an increased quantity and 
change of pressure, change of physical appearance such as cloudin 
increase of albumin, coagulability and the presence of abnormal sub- 
stances and micro-organisms. 

The pressure is increased in hydrocephalic conditions, whether due 



496 THE NON-NEURONIC DISEASES 

to tumor or meningitis, or other cause. It is not constant nor path- 
ognomonic in any way. Albumin is increased in the inflammatory 
conditions. 

The presence of blood may be accidental from the operation, or 
pathological. Hemorrhages into the brain and cord are the most fre- 
quent causes of it. 

Purulent meningitis often reveals pus cells in the fluid and ren- 
ders it cloudy. It is often cloudy also in tubercular meningitis. The 
presence of leucocytes may indicate purulent inflammation somewhere, 
though no pus cells are found. 

More important than all, however, are the bacteriological find- 
ings. These are not constant unfortunately, but when they are pres- 
ent a positive differential diagnosis can be made. The bacteria found 
are the bacillus tuberculosis in tubercular meningitis, the pneumococ- 
cus and meningococcus intracellular is in pneumonia meningitis, and 
the streptococcus and staphylococcus in purulent meningitis. 

DISEASES OF THE SPINAL COLUMN. 

These are practically all surgical disorders but they produce neu- 
ronic derangements of sufficient significance to warrant their consid- 
ation in a work upon neurology. 

DISLOCATIONS AND FRACTURES OF THE VERTEBRAE. 

The great majority of dislocations occur in the cervical region 
and are the result of blows and injuries of various sorts. In this way 
the atlas is displaced from the axis. Bone disease not infrequently 
causes dislocation between the fifth and sixth cervical vertebrae. Dis- 
placements are exceedingly rare in the dorsal and lumbar region.,, and 
when they do occur there do not give rise to marked nervous symp- 
toms. The displacement of the vertebra? may be in any direction and 
usually both adjoining bones are out of the proper line. The displace- 
ment may be unilateral ; as a rule, however, it is bilateral and may be 
complete or incomplete. 

Luxations in the cervical region may result from blows, twists, 
wrenches, falls and sudden turning of the head when there is a heavy 
weight being borne upon it. The deformity consists chiefly of an in- 
clination of the head forward, and of the spinous processes of the ver- 
tebrae below the luxated one backward. The chin thus is brought in 
apposition with the chest or shoulder and the occiput with the nape 
of the neck. Sometimes a noticeable prominence is to be detected at 
the side of the neck. Palpation at the back of the pharynx will some- 
times reveal the dislocation. The irregularity of the spines is always 
noticeable. 

The cord may be compressed, bruised or completely divided. The 
last is a very rare accident. A temporary paralysis caused by compres- 
sion may quickly disappear as soon as the dislocation is reduced. In 
the bruised cases there is some extravasation of blood and ere long 
myelitis. Quadriplegia, anaesthesia, sphincter paralysis and all the 



THE NON-NEURONIC DISEASES 497 

usual signs of transverse myelitis then appear and run their usual 
course. If the transverse ligament of the atlas is ruptured, as has 
occurred in hanging and in the lifting of children by the head, the odon- 
toid process may compress the spinal cord and produce instantaneous 
death. 

Fractures may occur in any part of the spinal column and be due 
to disease of the bones, associated with blows, falls, violent muscular 
contractions and sudden forcible flexion of the spine. The middle 
-cervical, upper dorsal and first lumbar vertebrae seem to be the choice 
victims of the accident. Dislocation often accompanies the fracture. 
Crepitation, fixation and distortion are the usual surgical symptoms. 
The cord is usually pressed upon and may be damaged even when there 
is no constriction of the canal. Rarely is the dura torn but there is 
almost always rupture of the veins and abundant hemorrhage in the 
extradural space. In the pia mater are slight extravasations of blood. 
The cord is usually bruised and compressed by the lower fragment. 
It is flattened and may even be completely severed. Rarely it has been 
lacerated longitudinally. Thus extravasation of blood and cavities have 
occurred in the cord substance. All of this is more or less localized. 
Immediately a myelitis lights up which may spread beyond the bruised 
area. Caries, sometimes of a secondary character, follows the injury. 

There are three great groups of symptoms in spinal fracture. 
There is the deformity. Then there is the general nervous shock with 
its sudden and temporary loss of consciousness, its vomiting and its 
pains and tetanoid manifestations. Lastly there are the signs of con- 
tusion, laceration and pressure of the cord. The last include the symp- 
toms of both epidural and subarachnoidal hemorrhage, central hetnato- 
myelia and transverse myelitis. 

The transmission of impulses through the cord is usually stopped 
by the focal damage. Motion and sensation are lost in those parts 
whose nerve supply is from the segment of the cord below the one 
that is injured. There is a horizontal or segmental distribution of the 
sensory phenomena, on the surface of the body. The upper edge of 
the sensory disturbance does not reach as high as the level of the af- 
fected vertebra. 

For the interpretation of the symptoms in these transverse, 
mental lesions, the reader is referred to the account of the Localiza- 
tions in the Spinal Cord. 

Sometimes the symptoms are not such as to afford an opportunity 
to make a segmental, localization diagnosis. They are irregular and 
anomalous. In such cases there is only partial damage of the cord 
and the confusion arises from the associated central hemorrhage in- 
juring the gray matter but leaving the white tracts uninvolved. 

In these transverse lesions, together with the motor and sensor} 
paralysis of all parts below the level of the lesion, there are 1<>>- of 
the reflexes in the zone of the lesion, or of the segmenl below it. and 
increase of the reflexes that have their central seal ^till lower down. 
Bastian's law, supported by Bruns, must be taken into account here. 
Bastian's hypothesis is that the lesion is only a partial one when there 
■are exaggerated reflexes below it. for he says that in all complete 



498 THE NON-NEURONIC DISEASES 

transverse lesions, the reflexes below are abolished. The functions of 
;he sphincters are always impaired. 

In all complete transverse lesions the paralysis in the limbs is a 
flaccid one. If the lesion is a partial one, it is spastic. All lesions in 
the lumbar region produce a flaccid paralysis in the legs. Disturbance 
of the sensibility with preservation of the general motor system means 
involvement only of the nerve-roots. Pains and twitchings, spasmodic 
jerkings, contractures and atrophic paralysis in the muscles innervated 
by the special nerves involved are then the objective phenomena. 

The clinical picture varies not only in accordance with whether 
the cord or roots are implicated and the degree of the damage done, 
but it varies as the lesion occurs in different parts of the column. 

Death is usually instantaneous in fracture of the atlas or axis. 
There may be a very slight displacement and the patient live, but he 
is in imminent danger from the slightest movement. Death usually 
occurs in such cases in a few weeks from secondary myelitis or even 
caries. 

Dislocation, inclination of the head, rigidity and immobility from 
pain, dyspnoea and bulbar symptoms are the usual signs of upper cer- 
vical fractures. In all cervical lesions the penis is erected; ejaculation 
takes place at the moment of injury; the temperature is elevated, the 
pulse increased and the general vasomotor apparatus disturbed. 

In mid-cervical fractures, the involvement of the phrenic nerve 
is a cause of death. Sometimes here there is only a slight displacement 
but there is constant danger from the slightest movement. 

Symptoms of the disease in the cervico-dorsal region are the 
oculo-pupillary disturbances with myosis and narrowing of the palpe- 
bral opening ; priapism ; vasomotor changes ; early paralysis of the 
legs and muscles of the trunk ; diaphragmatic respiration ; later in- 
volvement of the arms, affecting special muscles; muscular spasm and 
rigidity in the arms and hands ; and general hyperpyrexia. 

Dorsal lesions leave the arms intact and are usually accompanied 
by intense pains about the body and complete paralysis in the legs. 
Bastian's rule about the reflexes applies here, namely, that they are 
lost if the lesion is complete, exaggerated if it is incomplete. 

Lumbar lesions provoke a flaccid, atrophic paralysis in the legs, 
complete loss of reflexes, paralysis of bladder, rectum, genitals and 
anaesthesia in the distribution of the third and fourth sacrel nerves. 
This is the saddle type of anaesthesia. 

It is practically impossible to differentiate lesions of the Cauda 
equina from those of the conns mcdullaris, for the latter is surrounded 
by the roots of the former. There are radiating pains around the areas 
of distribution of the sciatic and pudendal nerves. 

The prognosis of all these cases is most serious. Dislocations 
hold out a better hope than do fractures. The latter often kill in- 
stantaneously or in a very short time. This is especially true of the 
cervical fractures. The lower dorsal and lumbar fractures may not 
at once destroy life but they set up spinal disease that causes bedsores, 
contracture, nephritis, cystitis and all the sequelae of a profound mye- 
litis that sooner or later does terminate fatallv. 



THE NON-NEURONIC DISEASES 499 

The management of these diseases is practically a surgical ques- 
tion. After careful study of statistics, Goldscheider formulates the fol- 
lowing practical conclusions : 

1. Recent cases should not be operated on, except where there is 
merely a comminutive fracture of the vertebra, fragments of which are 
pressing upon the cord. 

2. When the paralysis does not disappear and a deformity also 
exists, indicating a fracture of the vertebral body, an operation may be 
in place. 

3. Hemorrhage into the spinal canal is not a sufficient cause for 
laminectomy. 

4. Operation is more justifiable in fracture of the lower lumbar 
vertebrae than in any other region. 

CARIES OF THE VERTEBRA. TUBERCULAR SPONDY- 
LITIS. 

Pott's disease of the spine first attracted attention on account of 
the nervous manifestations produced by it. The old English surgeon, 
Percival Pott, described it as long ago as 1779. as a cause of paralysis. 
It is strictly a surgical, bone disease of tuberculous origin but which 
secondarily involves the spinal cord in such a way as to bring it most 
forcibly under the observation of neurology. 

Etiology. — A tuberculous cachexia underlies the disease, though 
in a few instances a non-tuberculous traumatic caries does occur. In 
many cases the tuberculous trouble lies dormant until an injury to the 
spine starts it into activity. There is an inherited diathesis often pres- 
ent and not infrequently tuberculous foci of disease are found in the 
lungs and other parts of the body. Sex seems to have no influence 
upon the incidence of the disease. It may appear at any age, though 
it is most frequently observed in childhood and early adult years. It 
does not always immediately follow an exciting traumatism for it is 
so insidious that many years may intervene between the injury that 
starts it and the first manifestations of its presence. It is now known 
that syphilis has nothing to do with it. Nearby centers of suppuration, 
as a retro-pharyngeal abscess may initiate a spinal caries. \ on-septic 
inflammation very rarely, if ever, causes it. Sometimes no cause can 
be found for it. 

Patholooy and Pathogenesis. — Usually only one vertebra is 
affected. Under the effects of a tuberculous osteitis, the body <>f the 
vertebra breaks down into a fungous, granulation tissue, eventuating 
even in the formation of liquefaction products, such as caseous and 
purulent matter. The bone softens and yields under tin- superincum- 
bent weight so that the spine is deformed and the cord is distorted or 
pressed upon. 'Hie inter-vertebral substance participates in the dis- 
ease process and like the body of the vertebra may go on to comp 
necrosis. The pus burrows in various directions. 

Xot infrequently, and especiall) under treatment, the disease pro 
cess ceases, resolution takes place, new hone replaces that which was 
lost, and a complete recovery is effected. 



5°° 



THE XOX-XEL'RONIC DISEASES 



The spinal cord is involved secondarily by compression and by 
the pns that oozes into the spinal canal. Sometimes there is an enor- 
mous accumulation of purulent matter between the cord and the ver- 
tebrae, involving the loose areolar tissue found there and the outer sur- 
face of the dura mater in a severe septic inflammation. When the 

FIGURE no. 




Pott's disease. (Whitman.) 

pressure becomes considerable the cord undergoes a similar inflam- 
matory process. A myelomalacia may first be produced by the com- 
pression and obstruction of the bloodvessels and lymphatics by the 
externa] pachymeningitis. Usually, however, a focal myelitis or men- 
ingo-myelltis occurs, which becomes more or less transverse though 
it does not extend longitudinally but a very short distance. 

The myelitic symptoms are typical and need not be described in 
greater detail here than to say that there is oedema, softening, prolifer- 



THE XOX-XEUROXIC DISEASES 5OI 

ation of the vessels, minute hemorrhagic spots and local secondary 
neuronic .degenerations. Occasionally the myelitic foci are dissem- 
inated. Inflammation always occurs when there is compression but 
sometimes it may appear when there is slight or no compression. In 
such cases it probably advances from the spinal nerve roots, a neuro- 
myelitis, or it may be the result of the extension of the disease along the 
course of the arteries, in which case the primary process may be a soft- 
ening from a tuberculous arteritis obliterans. The spinal roots of course 
are often affected. 

The dorsal cord seems to be the favorite seat of the trouble. The 
vertebrae being laterally displaced so that one is moved to one side in 
relation to its neighbor, or the bodies being collapsed, there is a notice- 
able deformity of the spinal column which often becomes very marked 
in the mid-dorsal region. One or two spines stand out beyond the oth- 
ers giving the typical appearance of an "angular curvature." 

• Symptoms. — The symptoms group themselves under the four 
heads of (i) constitutional manifestations, (2) the bone deformity, 
(3) the signs of involvement of the spinal roots, and (4) the signs of 
compression of the cord and myelitis. 

Usually the disease is so insidious that no constitutional or febrile 
symptoms are present. Signs of infection may appear, how- 
ever, but they belong to the tuberculosis or the general disease and 
are very variable. They need not concern us here as they are not a 
part of the spinal cord phenomena. 

In most cases there is a distinct spinal deformity. This is of the 
nature usually of a kyphosis. It is commonly known as Pott's hump. 
It is an acute angled protrusion or convexity backwards of the spinal 
vertebrae, due to the softening and yielding of their bodies to the 
superincumbent weight. It is accompanied by a local tenderness, and 
by which it has usually been preceded. The pain and soreness can 
be easily elicited by vertical pressure upon, and lateral movement of, 
the spines. When the disease is in the cervical region, movements of 
the head often provoke the pain. This of course produces a peculiar, 
half- voluntary rigidity of the neck and back that has a remote resem- 
blance to a torticollis. Deformity is not infrequently absent in cervical 
spondylitis. The tissues are thickened about the spine and a gravity 
abscess sometimes appears. These abscesses burrow and break out in 
all sorts of unexpected places. They often confuse greatl) the clinical 
picture. A retro-pharyngeal abscess, for instance, may interfere with 
swallowing so much as to lead one to imagine there is some bulbar 
paresis; or the abscess may follow the psoas muscle and appear well 
down upon the anterior part of the thigh. (Esophageal obstruction has 
been suspected from an abscess of spinal origin. 

The involvement of the nerve roots is witnessed by the charac- 
teristically distributed pains and their intensity. Sometimes the} 
absent. Not infrequently motor and sensory symptoms show the im- 
plication of both anterior and posterior roots. The pain, the hype 
thesia, the muscular weakness and the slight atrophy follow the course 
of the nerve distribution. A girdle-like sensation is thus produced. 



502 THE NON-NEURONIC DISEASES 

Instead of the hyperesthesia, there is occasionally a neuritic hyperaes- 
thesia, or even anaesthesia. 

The neuritic symptoms all occur only when there is a distinct 
pachymeningitis which, however, does not mean the majority of the 
cases. 

When the cord is implicated, the symptoms are usually those of 
a transverse myelitis, most frequently of the mid-dorsal type. There 
is a paraplegia of the legs with spasticity and exaggeration of the knee- 
jerks. If the cord is completely severed across by the destructive pro- 
cess the well-known exception of Bastian will be observed and conse- 
quently there will be flaccidity and loss of the knee-jerks in the lower 
extremities. Ancesthesia below the area innervated from the diseased 
segment of the cord is present. Above this a zone of hyperesthesia 
is often noticed. In this vicinity also occurs the girdle pain, so dis- 
tinctive a sign of myelitis. The superficial, like the deep reflexes of the 
lower limbs and lower part of the body are intact or exaggerated. 
Sometimes they are lost in accordance with PJastian's hypothesis. The 
vesical and rectal sphincters are paralyzed. Trophic symptoms occur. 
In brief, the entire clinical picture is that of a distinct transverse mye- 
litis. 

Oftentimes the existence of the caries is long recognized, some- 
times years, before the myelitic paralysis appears. The spinal deform- 
ity has been seen in early childhood and yet the paraplegia has not 
occurred until well into adult life. About a year or two after the 
kyphosis is discovered the paralysis supervenes. Occasionally both 
appear together. Rarely the paralysis has appeared without any ob- 
jective sign of bone disease for a time. 

The onset of the paraplegia is for the most part gradual though 
it has followed soon after some strain, injury or other exciting cause. 
In very rare instances it has been instantaneous, probably on account 
of some sudden displacement after a considerable period of bone dis- 
ease. Both legs are usually affected, though in some instances one 
leg has revealed weakness before the other. As a rarity, the Brown- 
Sequard syndrome may even be witnessed. 

The hump and tenderness in the spine, when observable, will help 
to localize the nervous lesion. But often these objective signs are 
not marked. Then we can often localize the trouble by the peculiar 
grouping of the nervous exhibitions. 

The nerve roots that are involved will be shown by the course 
and location of the pains, the peculiar distribution of the paralysis 
and atrophy, the hcrpetiform eruption, the hyperesthesia and the 
anaesthesia. In other words, the signs of a distinct, and local neuritis 
must be made out and then the origin of the particular nerves involved 
be traced back to the cord center. ( )f course these neuritic symptoms 
will only be observed when a pronounced pachymeningitis is in ex- 
istence. This is not often the case, however. 

This, as well as the localization of the lesion from the spinal 
cord symptoms, can be greatly facilitated by a reference to the table 
presented under the head of spinal localizations in the preceding 
chapte* 



THE NON-NEURONIC DISEASES 503 

If the damage is high up in the cervical region, there will be a 
spastic quadriplegia, without atrophy, with the paralysis more marked 
in the legs. Bulbar symptoms may be present with nystagmus and 
interference with respiration. Death under such circumstances may 
be imminent at any moment. The pains shoot up over the occipital 
region and there is a stiffness and half-voluntary fixation of the head 
that closely resembles a torticollis. Occipital anaesthesia may be de- 
tected. 

A lesion in the lower cervical area produces the well-known 
oculo-pupillary changes, sweating on one side of the head and vaso- 
motor disturbances. The legs remain in a condition of spastic para- 
plegia. The hands and arms undergo an atrophic paralysis which pre- 
cedes the trouble in the legs. There are sensory disorders especially 
in the ulnar distribution. The phrenic and spinal accessory nerves may 
be implicated. 

When the mid-dorsal region is the seat of the disease, the case is 
as a rule a typical manifestation of an ordinary transverse myelitis. 
The paraplegia with rigidity and increased reflexes in the legs, the 
sphincter disorders, the anaesthesia, the girdle pains and the decubitus 
constitute its tout ensemble of clinical presentations. 

As we approach the lumbar region, the paralysis of the legs be- 
comes flaccid in character and the knee-jerks are lost. 

These symptoms are subject to considerable variation in details, 
though when taken broadly as general groups they maintain a high 
degree of constancy, much more so than one would expect with such 
a variable lesion. As the myelitis spreads up or down the cord it in- 
volves this or that part more than another, symptoms appear that one 
may almost be inclined to regard as complications. Thus in old cases 
bedsores and cystitis occur. Poliomyelitic changes occur, causing 
profound atrophy and paralysis, with the classical electrical degenera- 
tive reactions. Implication of the posterior columns may lead to 
ataxic exhibitions. Pyramidal and disseminated lesions have been 
recorded with all their peculiar clinical manifestations. 

Diagnosis. — The readiness with which caries of the spine can 
be diagnosed is very different when the signs of bone disease are ob- 
trusive from what it is when they are absent. If there is a slight pro- 
trusion of the spine at one point and this is tender upon pressure or 
movement; if there are neuritic pains that seem to he in nerves that 
lead back to that point in the cord ; if the reflexes are slightly exagger 
ated, both skin and tendon reflexes; and if. especially, symptoms show- 
ing more or less solution in the continuity of the cord, as the spastic 
paralysis of the legs, anaesthesia, and irregularity ^\ the sphincters, 
the diagnosis can be made practically certain. The Rontgen raj may 
he brought into use to reveal an obscure hone lesion, but the u& 
tuberculin to establish the diagnosis is liable to be followed by dis 
trous results. If a focus of tuberculosis can he found elsewhere in 
the body, the diagnosis of course is strengthened, It must be remem- 
bered that traumata and other non-tuberculous causes can sometimes 
set up a simple spondylitis with similar implication of the nen 
structures. 



504 THE NON-NEURONIC DISEASES 

There are cases of caries in which the diagnosis is rendered very 
difficult by the absence of objective deformity. These cases can rarely 
be diagnosed with absolute certainty, though some of them are more 
than merely suspicious. If the patient is youthful and shows tuber- 
culosis elsewhere, together with a more or less localized set of slow, 
progressive nervous manifestations pointing to the cord or some of 
its nerve-roots, the diagnosis may be made with a fair degree of ac- 
curacy. 

If all signs of tuberculosis fail and we have nothing to depend 
upon but the nervous manifestations, the diagnosis becomes extremely 
difficult and uncertain. In such cases sometimes only waiting for 
further appearances will clear away the mystery. The disease under 
these circumstances is liable to be confused with primary myelitis, pro- 
gressive muscular atrophy, intercostal neuralgia, primary pachymen- 
ingitis, tubercular meningo-myelitis, intraspinal tumor, neurasthenia 
and hysterical paraplegia. Repeated careful examinations, with every 
effort made to elicit the slightest evidence of tuberculous bone dis- 
ease alone will enable one to establish the true character of these cases. 

Remember that in caries there are three great neurological fea- 
tures to be looked for, namely, a progressive, slowly advancing, fixed 
lesion, that first irritates and then destroys ; secondly, signs of nerve- 
root involvement such as the pains and atrophic paralyses ; and thirdly, 
signs of more or less severance of the spinal cord, with corresponding 
phenomena in all parts of the body below the lesion. Only in pachy- 
meningitis, primary myelitis, and tumor of the cord is this clinical array 
of events liable to be closely duplicated. 

In pachymeningitis the differential diagnosis is sometimes abso- 
lutely impossible. The usual causes of meningitis, especially syphilis, 
and the age of the patient must be taken into account. In pachymen- 
ingitis the cord symptoms are perhaps less and the root symptoms are 
more pronounced than they are in caries. 

Primary myelitis does not have the root symptoms to the same 
degree that caries has. The neuralgic pains and the local trophic signs 
are less pronounced. In a word primary myelitis is more distinctively 
a cord disease and exhibits the paraplegic, anaesthetic, girdle, sphinc- 
teric and trophic symptoms that go more particularly with cord lesions. 

In tumor the pains are more intense and excruciating, the pro- 
gression more steady and definite, and the succession of irritation and 
destruction more regular, as a rule, than they are in caries. 

In progressive muscular atrophy there are no pains and the 
atrophy is more systematically distributed. Moreover the extensive- 
ness of the symptomatology shows the greater extensiveness of the 
disease process. 

Intercostal neuralgia exhibits no atrophic paralysis, no cord symp- 
toms. 

Neurasthenic and hysterical patients not infrequently complain of 
spinal pains that might easily lead to a suspicion of tuberculous spondy- 
litis. In neurasthenia the spine is not often focally painful. It feels 
sore and heavy throughout its entire length. There are. moreover, 
no distinct organic manifestations such as caries almost invariably 



THE NON-NEURONIC DISEASES 505 

shows, to some degree at least. In neurasthenia the symptoms are those 
of fatigue and weariness and in a changeable sort of a way involve the 
entire nervous system. "Spinal irritation" as a unique condition, apart 
from the general neurasthenic state, has no place in modern neuro- 
logical nosology. 

In hysteria there are tender spots in the spine so frequently that 
I have long taught that they were almost pathognomic. They are mov- 
able, however, and are subject to the patient's mental changes. Hys- 
terical paraplegia is sometimes remarkably similar to organic paralysis. 
It is spastic; its reflexes are increased; the sensory symptoms are not 
as marked as is usually the case in hysteria ; and there may even be 
some muscular atrophy, probably from non-use. It is easy to com- 
prehend how this may be mistaken for organic disease. A Ye must de- 
pend entirely in such cases upon finding other hysterical stigmata and 
especially the mental status must be given close study. It is too fre- 
quent an error, however, which we should be warned of, the calling 
of an obscure case of caries one of hysteria. The treatment for caries 
would not hurt a hysteric ; the treatment for hysteria might bring irre- 
parable disaster upon a spondylitic case. I have seen a serious organic 
disease of the spinal cord several times made to pass beyond the repara- 
tive stage by its treatment upon the erroneous notion that the trou- 
ble was a mere neurosis. Caution is most imperative here and from 
my own observation of some of the sad errors that have been commit- 
ted, I am prone to feel that too much cannot be said in urging the pro- 
fession to keep their hands oft" of a case of spinal disease when they 
are in doubt as to whether it is an organic or a functional trouble. 

Prognosis. — The course of the disease is most variable and un- 
certain. The deformity may precede or it may follow the nervous 
manifestations. Steady progression or remissions may occur. Even 
sudden spontaneous and complete cessation may not be unlooked for. 
Abscesses are always liable to appear and in high cervical disease, bul- 
bar manifestations and sudden death need never cause surprise. w 
ter the paraplegic condition has declared itself, the myelitis is likely to 
terminate in about a year with the usual signs such as contracture, 
decubitus, nephritis, cystitis, and death. Occasionally the fatal issue is 
more the result of a general septicaemia and tuberculosis than <>f any 
special local trouble. When resolution and cure take place, either 
the cord manifestations or the spondylitic may vanish first. 

Youthful patients, and those in whom the disease has nol yet been 
of long standing, have a better chance both as to life and cure than 
aged and decrepit individuals and those in whom the history of the 
malady can be traced many years back. The existence of a general 
tuberculosis and the character and location of the abscesses modify, oi 
course, very seriously the prognosis. Mid-dorsal lesions offer the 
most favorable prognosis; high cervical lesions perhaps the worst. A 
case once got well after an attack of erysipelas, and I rowers mentions 
a complete recoverv in a case in which there- was paralysis of all tour 
limbs and the diaphragm. Serious as the disease is. therefore, on 
never justified in withholding hope of recovery from the patient and 
his familv. 



506 THE NON-NEURONIC DISEASES 

Treatment. — The two great indications for treatment are the 
bone disease and the secondary myelitis. 

For the tuberculous spondylitis a supporting treatment and pro- 
longed rest are the two great desiderata. The former involves rich, 
nourishing, fatty food, plenty of air and such well-established tonics 
as cod-liver oil and iron. The latter demands the recumbent position 
in bed ; best on the back because thereby the greatest amount of im- 
.mobility is obtained. Many months may have to be passed thus but 
the importance of the rest is so great that no temporizing should be 
allowed that in any way limits it. 

For the detailed treatment of the spondylitis the reader should 
consult the works upon surgery. Suspension, the wearing of a jacket, 
and the employment of revulsive measures will all be amply discussed 
there. Suspension seems to me to have too many disadvantages to 
cause it to be adopted as a routine measure. The cases that have ab- 
ruptly had their spinal symptoms relieved by it, have in all likelihood 
been cases with displaced vertebrae. The greatest disadvantage against 
it is that the rest, which is so necessary and which is more than any 
medicine or surgical procedure to the patient, is constantly broken. 
If the spinal extension could be maintained then the method would 
be both logical and commendable... A certain degree of permanent ex- 
tension is obtained by a jacket, a jacket with a jury-mast attachment 
and, better than all, a weight attached to the feet or to a band about 
the hips while the shoulders are drawn towards the head of the bed 
with sheeting passed under the arm-pits and around the bed posts. 
To be sure, not very great extension can be thus secured and it can- 
not be long maintained without wearying the patient. Its advantages 
are, however, that it can be easily accomplished without any disturbance 
in the recumbency of the patient. 

Except in a few cases, the plaster jacket had better be avoided. 
It causes much mobility in getting it on and off, and when once on 
it tempts the patient to go about more than is wise. An extension plas- 
ter-of-Paris bed, as suggested by Phelps and Lorenz, or even a suit 
of plaster-of-Paris proposed by Karewski, may not be objectionable 
for they at least infer the recumbent position. In my own judgment, 
however, the bed alone is the best, as necessitating the smallest amount 
of movement and yet furnishing a means of securing prolonged and 
absolute rest. 

The revulsive measures, such as setons, cautery and sinapisms, 
are not as much employed now as they were formerly. In regard to 
the more violent forms of counter-irritation I rejoice in this, but in 
regard to the steady, prolonged use of mild counter-irritation I think 
we may lose a valuable aid to the treatment, if it be entirely discarded. 
The continuous application of weak mustard plasters or mustard poul- 
tices may not do much for tuberculous spondylitis, but I am sure it 
has in my hands helped very greatly, and more than once, the spinal 
inflammation. The skin must not be damaged, the sinapism must be 
shifted about, and the treatment must be prolonged for weeks and 
months. Cupping, wet or dry, is an abrupt treatment and has more 
disadvantages than advantages. 



THE NON-NEURONIC DISEASES 507 

Operative procedures, such as laminectomy, forcible redressement, 
have not gained popular favor because their later results have not been 
so favorable as they promised to be at first. These are surgical ques- 
tions, however, and their discussion does not belong here. 

There is no specific treatment for the disease process. Oleum 
morrhuse and iron about exhaust the list. The syrup of the iodide 
of iron is particularly useful. Mercury and the iodides would of 
course come into play if there is a history of syphilis. I consider the 
calcium salts as very much over-rated. I have administered them 
time and again without seeing the results that others have claimed for 
them. 

The treatment of the nervous lesions is fostered by the treatment 
.given for the tuberculous bone trouble. In fact, after the bone disease 
has disappeared the nervous trouble often vanishes also. If compres- 
sion merely is present, the entire management of the case resolves 
itself into the management of the bone disease. If myelitis is present, 
the treatment, secondary to that of the bone trouble, should follow the 
.general principles laid down for that of inflammation of the cord. 
Symptomatic treatment is of the greatest importance in combating the 
"bedsores, the cystitis, the contractures. In the cases that recover, mas- 
sage and mild faradic stimulation of the muscles may be of use. Tenot- 
omy may be called for to counteract the deformities produced by the 
contractures. 

In mentioning electricity, I desire again to emphasize the fact 
that it is a most dangerous agent if improperly used. I have sometimes 
wished it had never been introduced into general therapeutics. With 
some medical men, and nearly always with the laity, nervous diseases 
are always the indication for electrical treatment. If the trouble is 
spinal and they don't know just exactly what it is, they at once be- 
gin the use of strong galvanic currents up and down the spinal cord. 
I would like to see such practices made a crime. I have been the un- 
willing witness of them several times. Electricity is rarely, if ever, 
called for in spinal or brain diseases. It is most religiously contra- 
indicated in organic acute diseases and where there is a possible doubt 
about the accuracy of the diagnosis. To see a mild, stationary myelitis 
that interfered but little with the patient's comfort suddenly trans- 
formed into a complete paraplegia, with a rapid hastening of the pa- 
tient toward death, by a medical man who gloried in the use of his elec- 
trical paraphernalia, but who could not distinguish a myelitis from a 
rheumatism, is a most disheartening and exasperating experience. 

Patients that have once had caries n\ the spine must lead a care- 
ful, hygienic life and must be warned of the possibility of relapse from 
a neglect to do so. 

TUMORS OF TIM': VERTEBRAE. 

Carcinoma, sarcoma and myxoma are the principal new growths 
that attack the spinal column and secondarily affect the spinal cord 
and its functions. Exostoses growing from tin bodies of the vertebrae 
into the spinal canal may also produce very slow, progressive cord 



508 THE NON-NEURON 1C DISEASES 

symptoms. Of all these, however, cancer and sarcoma are the most 
common. The same conditions for all of them are usually found else- 
where in the body. Carcinoma especially is generally due to the same 
disease in the stomach, womb, mammary gland or other organ from 
which it has spread by metastasis. Sarcoma and osteosarcoma spread 
from the surrounding parts and are found chiefly in those advanced 
in years. Rarely are any of these growths primary in the vertebrae, 
though when they are primary they usually start in the bodies and 
spread from one to the other. The vertebral bodies break down and 
thus allow the formation of an angular curvature. This kyphosis is- 
not generally so sharp as it is in caries, as more bones take part in it 
and the tumor is present to modify it. 

From the bodies there may be an extension of the growth into 
the neighboring ribs, muscles, along the lateral processes of the corre- 
sponding vertebrae, narrowing the inter-vertebral foramina through 
which the spinal nerves pass. The nerve roots are pressed upon, in- 
flamed and sometimes infiltrated by the cancer. The disease may even 
advance into the areolar tissue between the dura and the vertebrae and 
surround the cord completely. The cord is thus compressed and often 
inflamed. It is never invaded, however, by the neoplasm. 

The nervous symptoms of special import are the intense pains 
from the implication of the posterior nerve roots and the signs of com- 
pression of the cord. Most cases are diagnosed from the deformity of 
the spinal column, the presence of the disease elsewhere in the body and 
these nerve root manifestations. 

The pains follow the course of the spinal nerves and are distinc- 
tive for their excruciating intensity. They are far more intense than 
they are in caries. At first' there are remissions but later on they are 
constant with paroxysmal exacerbations. They are sharp, lancinating 
and are increased by every movement. They appear in the arms, 
trunk, and legs, according to the site of the tumor. They are accom- 
panied by cutaneous hyperaethesia and spots of anaesthesia. The asso- 
ciated muscles are thrown into a state of spasm and rigidity, are con- 
tractured, paralyzed and wasted. Spasms and pains often appear to- 
gether in the paroxysms. In some cases paraplegia develops, often 
very rapidly. In this the cord manifestations differ from those of 
caries, where they progress more slowly. Twelve or twenty-four hours 
may see all power in the legs lost. The intensely painful character of 
this paralysis led Cruveilhier to name it paraplegia dolorosa. Some- 
times the onset of the paralysis is slower. The compression of the 
cord is the explanation of it. There is nothing distinctive about the 
paralysis. Inflammation more often accompanies it perhaps than it 
does the paralysis of caries. 

The diagnosis should carefully take into account the age of the 
patient, the presence of the disease in other parts of the body, the spinal 
deformity, the intense character and anatomical distribution of the 
pains, and the signs of compression of the spinal cord. Skiagraphy 
may be invoked to assist the diagnosis. Caries is less painful, is tuber- 
culous in the vast majority of cases and occurs in younger individuals. 



THE NON-NEURONIC DISEASES 509 

Jn intercostal neuralgia the pains are not bilateral and there are no mo- 
tor or cord phenomena. 

Cancer is a growth that often runs its course in a few months. 
The other tumors last for years and then destroy life only secondarily 
.by the trophic troubles they set up and the intercurrent maladies that 
intervene. 

The prognosis of course is always bad. 

The operative treatment so far has not accomplished anything. 
Morphine to relieve the pains and general hygiene is about all that can 
be done. 

SYPHILITIC DISEASES OF THE VERTEBRAE. 

Syphilitic exostoses that press upon the cord are not common. 
They produce deformity or rather a spondylarthrosis ; damage the 
nerve-roots ; and compress the cord. There is, therefore, nothing dis- 
tinctive about them but their etiology. This is usually clear. If it is 
only suspected it may be cleared up by the administration of the iodides 
in large dosage for a long period of time. 

ANEURISMAL EROSION OF THE VERTEBRAE. 

This cannot be diagnosed unless there are other indications in 
the body of aneurism. Symptoms of a neoplasm such as I have been 
relating, involving the nerve-roots and the cord, that are suddenly in- 
terrupted by a complete paraplegia followed by an ascending paralysis, 
would justify a strong suspicion of a ruptured aneurism within the 
spinal canal. The condition is of more pathological then clinical in- 
terest. 

SPINAL HYDATID DISEASE. 

Leyden and others have collected a number of reports of the de- 
velopment of hydatid cysts in the areola tissue between the cord and 
the bones, and possibly even in the bones themselves. Double cysts, 
partly in and partly outside of the canal, have been observed. ( H 
course the cord is compressed and inflamed, with the usual symptoms. 
The diagnosis is extremely difficult from other vertebral diseases that 
provoke a similar clinical picture. We can only depend upon the pres 
ence of the disease elsewhere. Practically all cases prove fatal, even 
though puncture has been tried as a means of amelioration. 

LATERAL CURVATURE OF THE SPINE. 

This rarely, if ever, produces distinct ennl symptoms, even when 
there is slight pressure. I have seen it. however, ran.se decided weak 
-ness in the legs, neuralgic pains and severe general neurasthenic man- 
ifestations. The accompanying picture is thai of a girl who was a 
sufferer from such symptoms and supposed she was a nervous wreck. 
A correction of the spinal deformity resulted in her complete restora 
tion to health and happin 



5io 



THE N0N-NEUR0NIC DISEASES 



ARTHRITIS DEFORMANS OF THE SPINAL COLUMN. 

As a phase of the disease rheumatoid arthritis, the articulations be- 
tween the vertebrae may be affected and even become anchylosed. The 
whole spine may be involved but it occurs more frequently in the cerv- 
ical region. The inter-vertebral cartilages undergo atrophy or become 
calcified, the heads of the bones become enlarged, new bony formation 

FIGURE in. 




Lateral curvature of the spine with marked hystero-neurasthenic symptoms. 
Orthopaedic treatment for the spinal trouble caused complete disappearance of 
the neurotic manifestations. 

takes place on the spinous processes and complete fixation occurs. The 
Spine is thus made rigid. The neck becomes fixed and the chin is in- 
clined toward the chest. The inter-vertebral foramina are constricted 
and the nerves pressed upon. The spinal cord is not usually impli- 
cated. A descending neuritis is seen in some of the nerves involved. 

The symptoms of the disease include the rigidity of the spine, which 
does not yield under chloroform narcosis, local tenderness in the spine, 



THE NON-NEURONIC DISEASES 5II 

radiating pains and a partial neuritic atrophic paralysis in the area to 
which the nerves go that are inflamed. The inflamed nerves are lo- 
cally tender, as well as being the seat of the shooting, lancinating pains. 
The sympathetic may be implicated when the trouble is in the cervical 
region. The nerves of the medulla have been affected in a few in- 
stances. The diagnosis of the malady must be made largely from the 
presence of the same disease in other joints of the body. 

The disease is a chronic one, running its course with remissions 
and exacerbations. It is incurable. The best we can do is to foster 
a remission by the use of massage, local applications of iodine, the 
administration of potassium iodide, the salicylates, quinine, iron and 
arsenic, and the employment of sulphur and alkaline baths. 

DISEASES OF THE MEMBRANES OF THE SPINAL CORD. 
ANJEMIA AND HYPEREMIA. 

Notwithstanding the fact that many of the older neurological 
writings contain much about anaemia and hyperemia of the spinal 
membranes, we know practically nothing about these conditions. ( )n 
account of the peculiar arrangement of the circulation and its rich 
anastomoses in and around the spinal cord, it may well be doubted 
whether anaemia or hyperaemia of the membranes ever occurs apart 
from a similar condition in the cord. Of the possibility of the latter 
there is not a little dispute. It is not intended by this to deny abso- 
lutely that anaemia follows a severe hemorrhage, an exhaustive diar- 
rhoea or an aortic obstruction, or that a hyperaemia is associated with 
certain sexual and muscular excesses, uraemic and other convulsions, 
suppression of menstruation and strychnine poisoning. It is but to 
reiterate that we do not have any positive knowledge of such an under- 
lying condition. It must be presumed that in the earliest stage of 
meningitis, and possibly as a residuum after the inflammation, hyperae- 
mia of the membranes exists for a time. 

The clinical description of these conditions is full of obscurity. 
On the one hand many of the symptoms referred to by authors are too 
subjective in character to possess any value as indications of a gross 
pathological disturbance; and on the other hand they are very closely 
like those that are known to be indicative of actual inflammation in 
the membranes. The heavy feeling in the legs, the weakness amount- 
ing to paraplegia, the pains in the back, and the supposed relief afford- 
ed by lying flat on the back, are too indefinite and certainly too posi- 
tively assumed, as indications of aiucmia. Such a pathology was ai 
one time adopted for spinal concussion and the traumatic neuroses; bu1 
in addition to what Page and others have done t<> show tin- untena- 
bility of such a pathology, we now know- that the traumatic neuro 
including railway spine, railwa\ shock and spinal concussion, are 
mostly cases of hystero-neurasthenia. 

The same general critcism is to he made of the clinical descrip- 
tion of hypercemia. the heaviness and weight in the limbs, the numb- 
ness, the slight paresthesia, the fugitive pains, the muscular twitch- 
in gs, the disturbance of the sphincters, and the asserted relief obtained 



512 THE NON-NEURONIC DISEASES 

by lying on the face or side, are too subjective in character to be of 
real symptomatic value ; or are much like the well-recognized symp- 
toms of actual inflammation. At all events the clinical picture usually 
accredited to spinal hyperaemia has not yet been sufficiently identified 
with such a pathological basis. 

All of which being so it is useless to discuss further the diagnosis, 
prognosis or treatment of anaemia or hyperaemia of the membranes. 

INFLAMMATION OF THE SPINAL MEMBRANES. SPINAL 

MENINGITIS. 

Of the three membranes covering the spinal cord, two, the dura 
mater and pia mater, undergo distinct forms of inflammation. The 
arachnoid becomes implicated with the other two. Only in very ex- 
ceptional instances does the inflammation confine itself entirely to the 
membrane originally attacked. Sooner or later the neighboring struc- 
tures are involved by contiguity. Thus when the dura is inflamed 
externally the bone above it has usaully been damaged and the loose, 
connective tissue between it and the bone is involved. When it is 
inflamed internally the arachnoid and pia are almost certain to be in- 
cluded. When the pia is the original seat of the disease, the arach- 
noid above it, including sometimes the dura, and the outer edge of 
the cord below it, are as a rule more or less implicated in the same 
process. 

This disease process may be primary or secondary, simple or 
purulent, acute or chronic. The symptomatic manifestations may van- 
greatly, the variations depending upon the character and location of 
the inflammation. A number of types of spinal meningitis, therefore, 
are recognized. Involving the dura mater we distinguish an acute 
and chronic external, and an acute and chronic internal, pacliyiucn- 
ingitis. 

The inflammation of the pia mater is known as acute and chronic 
leptomeningitis. 

Chronic syphilitic meningitis is sometimes spoken of as arachnitis 
gummosa. 

The forms of the disease deserving of further consideration by 
reason of their clinical importance are external pachymeningitis, hem- 
orrhagic and hypertrophic internal pachymeningitis, acute leptomen- 
ingitis, and chronic syphilitic meningitis or rueningomyclitis. The 
epidemic form of cerebrospinal meningitis will not be discussed here. 

EXTERNAL PACHYMENINGITIS. 

This form of spinal meningitis never occurs de novo. Tt is a 
secondary inflammation. 

Etiology. — Tuberculosis and caries of the vertebrae, fractures 
and dislocation, septic processes and purulent inflammations in other 
parts of the body, such as purulent pleurisy, psoas abscess, puerperal 
pyaemia, are the causative factors in external pachymeningitis. 

Pathology. — A purulent inflammation with exudation and pus 



THE NON-NEURONIC DISEASES 513 

in most cases occupies the space between the bone and outer surface 
of the dura. The latter is covered with a thick, creamy, fibrinous ex- 
udation either of pus or caseous matter. The dura itself is thickened. 
The inner surface of the dura is often implicated, but the underlying 
pia very rarely so. The inflammatory process is more marked poste- 
riorly than anteriorly on account of the peculiar arrangement of the 
bloodvessels. The cord itself is compressed, flattened, and in excep- 
tional cases may show some degree of peripheral inflammation. The 
thickened membrane surrounding the nerve-roots constricts them and 
causes them to undergo inflammation, softening and atrophy. All of 
this produces what is sometimes called compression myelitis and multi- 
ple neuritis of the nerve-roots. As a rule the disease extends focally 
along a certain distance, though at times the whole membrane may 
be involved. The cervical part is not as frequently attacked as the 
dorsal and lumbar on account of the close attachment of the dura to 
the bone in the neck. The cellular tissue between the dura and the 
bone is sometimes purulent throughout the entire length of the canal. 

Symptoms. — The symptoms of external pachymeningitis are oft- 
times inextricably confused with those of the original disease. When 
they can be clearly distinguished they are the signs of irritation and 
compression of the cord and- nerve-roots. The spine is tender and 
painful, especially over the focus of the disease. Every movement 
causes pain. Pains shoot down the limbs and around the trunk. These 
radiating pains may assume the form of typical girdle, constricting 
bands. The pains show a tendency to follow anatomical lines of nerve 
distribution. Various parccstliesicc are present in the extremities, such 
as numbness, formication, pins-and-needles sensation and tingling. 
Hypercesthesia of the skin is common. Among the motor manifesta- 
tions are twitchings of the limbs, various degrees of paresis, partial 
paraplegia. The reflexes are generally exaggerated and the sphincters 
may be incompletely affected. If the disease process is limited in ex- 
tent, its location will modify the symptomatology somewhat. When 
the cord is inflamed myelitic symptoms may appear. The tempera- 
ture, respiration and pulse rate will ail assume their characteristics 
very largely in accordance with the extent and nature of the original 
trouble that is the cause of the pachymeningitis. 

Diagnosis. — When there is a history of injury or other disease 
of the spine, or of suppurative processes elsewhere, the above general 
•clinical picture will make the diagnosis easy enough. Myelitis is de- 
void of the general history of these cases, does not have the same sort 
of rachialgia and radiating pains, nor the temperature, but on the 
other hand is the cause of more complete paralyses, trophic and vaso 
motor disturbances and distinct focal signs. There are no radiating 
pains, paramnesia and histor) of injury and suppuration in muscular 
rheumatism. Tetanus is distinguishable by its trismus and the excita- 
tion of the muscular spasms by peripheral irritation. 

Prognosis. — This is always grave. It depends upon that of the 
original disease, as well as upon the character of the meningeal in- 
flammation. If the original trouble were not serious, and the menin- 
geal symptoms indicated only irritation, some hope of recovery might 



514 



THE N0X-XEUR0XIC DISEASES 



be held out. When the original trouble is serious, as it mostly is, and 
especially when the meningitis has been of long standing, showing 
involvement of the cord, the prognosis is absolutely bad. 

Treatment. — The treatment is practically surgical and concerns 
itself mostly with the primary disease. This once overcome, the men- 
ingitis is to be treated upon the same principles as any of the more 
common forms of the disease. 



CHRONIC CERVICAL HYPERTROPHIC 

G1TIS. 



PACHYMENIN- 



This is an internal inflammation of the dura mater, chronic in 
duration, hemorrhagic and hypertrophic in character, and involves 
sooner or later the adjoining arachnoid, pia and cord. It was first de- 
scribed by Charcot and Joffroy. 

Etiology. — Adults are usually affected by this disease, though 
cases have been reported in children. Males are more prone to it than 
females. Cold, trauma, over-exertion, exposure and alcoholism have 
been said to produce it. Syphilis, however, plays so large a role in its 
etiology, that some have wondered whether the disease were not a 
manifestation of spinal syphilis. It has been supposed to have been 
brought on also by syringomyelia. In the hemorrhagic form, analogous 
almost to the hematoma of the cerebral dura, it is not uncommon in 
the chronic insane. 

Pathology. — The disease is most frequent in the cervical re- 
gion, though rarely it may occur in other parts of the column. The 
most striking pathological feature is the thickening of the dura, almost 
five and ten times as thick as the normal membrane. The process is 
a chronic one, is more or less limited to the internal layer of the dura, 
and ultimately involves the underlying arachnoid, pia and cord. Pre- 
ceding the hypertrophic process, in most cases, is the hemorrhagic, 
which in a way resembles a dural hematoma such as occurs on the 
brain sometimes. The hemorrhage occurs on the internal surface of 
the dura and is followed by a chronic inflammation. After a time an- 
other hemorrhage with inflammatory action and deposition of new mat- 
ter takes place. By the frequent repetition of this pathological action, 
layer after layer of fibrinous tissue is deposited, gradually thickening, 
hardening, almost ossifying the membranes, binding them together 
and constricting and compressing the spinal cord and nerve roots and 
thus producing in the latter atrophy and sclerosis. In the syphilitic 
cases the deposited material is of the gummatous variety. As a result 
of the steady compression and the extension of the disease into the 
substance of the cord, the latter becomes involved completely across. 
Even cavities may form in it. 

Symptoms. — A moment's consideration of the nature and progress 
of the lesion in this disease will enable one to quite definitely 
foretell the character and succession of the symptoms. There are quite 
distinctly three sets of symptoms which follow one another in a regu- 
lar progression. The first set of symptoms indicate irritation of the 
cord and roots. There is pain in the neck and stiffness. Pains are 






THE XOX-XEUROXIC DISEASES 



L 



felt in the back of the head and between the shoulder blades. The 
vertebrae are tender upon percussion. Hyperesthesia and paresthesia 
occur, especially down the arms and usually more in one arm than 
the other. Numbness, tingling, pricking, are complained of, especially 
along the area of distribution of the ulnar and median nerves. The 
sensory symptoms and particularly the pains are apt to be worse at 
night. Muscular rigidity, cramps, tremor indicate the motor irritation 
in the arms and hands. All of these symptoms continue for many 
weeks or months before the next stage comes on and are obviously due 
to the meningitis. There may be some slight disturbance of tempera- 
ture and pulse, of the irregular type. Xausea and vomiting are not 
entirely unknown. 

Following this neuralgic stage is the second or paralytic, which 
is purely neuritic in character. The arms are chiefly affected. They 
are weak, rigid, contracted and atrophied. The extensors being unop- 
posed by the normal action of the flexors, there is over-extension of 
the wrist. The fingers are over-extended in the basal phalanges, 
sharply flexed in the middle and end phalanges. This gives an almost 
pathognomonic appearance to the hand, known as the preacher's hand, 
or main- en- grift : e. This paralysis is of the degenerative type and is 
most pronounced in those muscles supplied by the ulnar and median 
nerves. Other nerves of course may be involved, as, for instance, the 
radial, causing pronation. The pains, anaesthesia, hyperesthesia and 
trophic manifestations continue during this stage. In some cases it is 
in this stage that the oculo-pupillary symptoms become marked. There 
may be dilatation followed by contraction. The pupillary signs, how- 
ever, are not distinctive in any way of the disease. This is a very 
chronic stage, even more so than the first. Its symptoms are plainly 
due to the severe compression and beginning destructive inflamma- 
tion in the roots and peripheral border of the cord. It is not sharply 
defined from the last, or paraplegic stage. 

In the third stage, the paraplegic, the cord is more or less diseased 
and damaged completely across. The pains and other sensory symp- 
toms now gradually decrease as the paralysis of the legs comes on. 
This paralysis is spastic in character and is associated with exagger- 
ated knee-jerks, increased myotatic irritability, muscular rigidity and 
spinal trepidation. Anaesthesia is present, as well as disturbance of 
the sphincters. Gradually weakness and exhaustion supervene and the 
patient dies of this or some intercurrent malady. 

The clinical picture of the disease which I have just presented is 
of the more common, cervical type. The extension of the inflamma- 
tion up or down the cord will of course modify the picture somewhat. 
Involvement of the medulla and pons will add corresponding symp- 
toms, such as impairment of hearing, tachycardia, and other special 
bulbar manifestations. In the so-called peripheral type of the di» 
the symptoms are more distinctly limited and localized in the extrem- 
ities. 

Diagnosis. — The diagnosis of cervical hypertrophic pachymen- 
ingitis is at times extremely difficult. At first it may be mistaken for 
Pott's disease of the spine. Later on the atrophy of the muscles may 



5 J T> THE NON-NEURONIC DISEASES 

lead to the erroneous opinion that the case is one of progressive mus- 
cular atrophy. And still later, the syringomyelic lesion added to the 
pachymeningitis will be sure to lead to confusion. Moreover the dis- 
ease has to be carefully differentiated from myelitis, spinal tumor, tor- 
ticollis, etc. 

When the disease is of the typical, cervical type, the localization 
of the symptoms, their bilaterality, their chronic, progressive charac- 
ter, their more or less agreement with the succession of stages out- 
lined above go far toward making the diagnosis positive. At times 
tumor cannot be differentiated. The safest way to differentiate this 
from other typical diseases is to exclude this by a careful considera- 
tion of all of the symptoms of the others. A myelitis, for instance, is 
not preceded as a rule by a prolonged meningitic period and a pro- 
gressive muscular atrophy is practically devoid of all sensory phe- 
nomena. 

Widal and Le Sourd have suggested that an examination of the 
cephalo-rachidian fluid should be made in doubtful cases. In Pott's 
disease, for instance, this fluid is normal with respect to its cellular 
contents, whereas in pachymeningitis it contains after centrif ligation 
mononucleated elements, lymphocytes for the most part, mixed with 
some large cells having a single nucleus and much protoplasm. 

Prognosis. — This disease is painful, chronic and progressive. Its 
progress may cease at any stage. Cure has been occasionally reported. 
Most of the cases, however, terminate in death and a grave prognosis 
had better always be given. 

Treatment. — Syphilitic cases of course should be vigorously 
combated with mercury and the iodides. Other cases may be helped 
by the use of local counter-irritation. Iodine, mustard, cups, the act- 
ual cautery, are all indicated. Hydrotherapy has seemed to have been 
useful in a few cases, in giving relief if not in producing a cure. The 
pains, spasms, etc., must be treated symptomatically with anodynes, 
narcotics, antispasmodics. Electricity has a field of usefulness here 
apparently and is worthy of a trial. It is not impossible that sur- 
gery may be of some benefit to these cases some day. The indications 
are suggestive and if undertaken early enough, before there is serious 
involvement of the cord, lumbar puncture, laminectomy, or incision of 
the dura may accomplish something favorable. 

VCUTE SPINAL LEPTOMENINGITIS. 

This is an acute inflammation of the pia mater, rarely occurring 
apart from cerebral meningitis, is secondary, and is due to infection. 

ETIOLOGY. — Simple, primary leptomeningitis is practically un- 
known. When due to a traumatism, to rheumatism, exposure and sun- 
stroke it is nevertheless infective in origin. It occurs in tuberculosis, 
syphilis, typhoid fever and septicaemia following purulent wounds, 
otitis and the puerperium. It is the form of meningitis that occurs 
epidemically as cerebrospinal meningitis. Children are the most fre- 
quent sufferers, and among adults males predominate. Dana remarks 
that alcoholism predisposes to it. 



THE NON-NEURONIC DISEASES $IJ 

Pathology. — The character of the inflammation and its accom- 
paniments will naturally depend upon the cause and infective character 
of the original disease. Syphilitic cases reveal the gummatous, gran- 
ular exudate. In the tuberculous cases there is not a very abundant 
exudate and it is of a fibrinous nature, grayish in appearance. Pus 
of course is absent, but there are miliary tubercles in the meshes of 
the arachnoid and on the inner surface of the dura. Simple exudative 
meningitis is so rare as to be of but little clinical interest. In most 
of the cases an exudate is found that is due to various pyogenic micro- 
organisms such as the streptococcus pyogenes, to the pneumon- 
coccus, etc. Thus an initial hyperemia is followed by a purulent exu- 
dation which spreads through the pia and arachnoid and clouds the 
cerebrospinal fluid. The membranes are bound together by adhesions 
and adhere closely to the cord. The spinal nerve-roots and the peri- 
phery of the cord are constricted and slightly inflamed. All of this 
is more marked on the posterior than the anterior or lateral aspects of 
the cord. Sometimes the disease localizes itself focally at various 
levels. When the inflammation ends there is often left a mass of new 
connective tissue, or the disease passes into a state of chronicity. This 
causes sclerotic changes and by the compression, irritation and destruc- 
tion caused by the thickened, adhering membranes keeps alive a group 
of subacute, permanent symptoms. 

Symptoms. — The chief symptom of spinal meningitis is pain, and 
is the result of pressure. The pains are local and radiating, dull, 
aching, sharp and shooting. The spine itself is tender on pressure and 
percussion. The tenderness occurs sometimes in spots, these spots 
usually overlying the foci of maximum inflammation. Sharp, shoot- 
ing pains are felt up in the neck and back of the head, down into the 
arms, around the trunk and down along the legs. They follow the 
course of the nerves and are due to the compression and constriction 
of the posterior nerve roots. The same pressure and irritation of the 
anterior roots cause muscular rigidity. The muscles of the back and 
neck are stiff. The body is sometimes thus bowed forward in the con- 
dition of opisthotonos with the head boring backward into the pillow. 

All this usually starts abruptly with a chill, some deration of 
temperature and alteration of the pulse rate. There may be a Febrile 
headache and other indications of cerebral meningitis with nausea and 
vomiting. The urine is retained and the bowels are constipated. 
Gradually the pains increase as well as the muscular stiffness. As 
every movement of the back provokes pain, the patient adds his volition 
to the maintenance of the muscular rigidity. The skin is exceedingly 
hyper (Esthetic and painful. The relieves an- increased at first, but 
diminished later on. On account of the muscular stiffness, Kerui^'s 
sign is present. The so-called tdche bleudtre of the French writers 
can be elicited and indicates implication of the vasomotor apparatus. 
It is not important, however. 

If the patient is not cut off early by death, paralysis, paraplegia 
or paraparesis will usually come on. The sensibility becomes 
sened, the bladder grows weak and the relieves become profoundly 
affected. The respiration, the heart beats and the pupillary activity 



518 THE NON-NEURONIC DISEASES 

may all be implicated. In the last stages complete palsy, atrophy and 
anaesthesia may be observed. The most severe and rapid onset of 
symptoms outlined above occur in the septic cases. 

The tuberculous forms of the disease are slower in their onset 
and progress, while the infectious forms range between the septic and 
tuberculous in this respect. 

Diagnosis. — The diagnosis of spinal meningitis is not difficult. 
The febrile symptoms, the local tenderness and radiating pains, the 
tonic and clonic spasms, the Kernig and reflex signs, when all placed 
together produce an unmistakable picture. In myelitis there is no 
spinal tenderness and generally less pain but much more pronounced 
paralysis. The sphincters are affected in myelitis, the reflexes are 
characteristically exaggerated and the trophic manifestations are more 
prominent. In tetanus the history of an injury, the trismus and the 
absence of the irregular, high fever of meningitis, ought to make a 
differentiation comparatively easy. Rheumatism exhibits mere mus- 
cular pain, no cutaneous hyperesthesia, bladder symptoms or trophic 
manifestations. The examination of the cerebrospinal fluid obtained 
by lumbar puncture may be resorted to in very doubtful cases. It 
will show in nearly every case a cloudiness, and a leucocytosis, and pos- 
sibly a few bacilli. 

Prognosis. — The onset and course of the disease are generally 
acute and foudroyant. In a few days it generally proves fatal ; hence 
the prognosis is, as a rule, bad. Sometimes the patients linger several 
weeks before death overtakes them. These cases may subside and 
pass into chronic meningitis. The cases with the worst prognosis are 
those with high fever, intense pains and rapid appearance of paralysis. 
Septic cases are bad and the tuberculous cases, though ofttimes slow 
and prolonged, cannot be expected to recover. Very rarely, however, 
recovery has occurred ; more particularly among the epidemic and 
otitic cases. Partial recovery, with a remaining bladder weakness, 
slight paralysis, hyperesthesia may legitimately be always hoped for. 

Treatment. — The first thing to do in the treatment of spinal 
meningitis is to put the patient's mind and body at rest. Perfect 
quietude of room and environment must be obtained. The pains must 
be suppressed by opiates, and sleep be induced by bromides and other 
hypnotics. The skin, bowels and kidneys should all be made as active 
as possible and with the least amount of disturbance of the patient. 
As the patient is urged to lie most of the time on the side or abdomen, 
local treatment of the spine can easily be instituted and carried out. 
An ice bag, of the Chapman type, may be placed alongside of the 
spine, or wet packs may be similarly employed. After the pain is 
lessened somewhat, dry cups, leeches and sinapisms may be used. I 
do not favor too energetic measures for they are apt to irritate and 
disturb the patient. In most of my cases I use mustard, even diluted 
with flaxseed, daily or twice a day on alternate sides of the spinal ver- 
tebrae. I believe more is accomplished by constant prolonged mild 
counter-irritation than by too hasty or severe methods. 

Notwithstanding some opinions to the contrary. T am satisfied that 
mercury is the best medicament now at our disposal for the internal 



THE NON-NEURONIC DISEASES 519 

treatment of spinal meningitis, syphilitic as well as non-syphilitic. It 
may be used by inunction or by the mouth. Any preparation of mer- 
cury may be used, though I prefer unguentum hydrargyri, calomel or 
blue mass. It must be given rather freely, guarded by opium, and 
for a long period continuously. I have not found it necessary to ex- 
periment with small doses of potassium iodide or sulphate of magne- 
sium, given at short intervals, though both are highly indorsed. In 
the later stages of the disease more heroic counterirritation by means 
of cantharides, the hot iron, the Paquelin cautery, or even mere hot 
douches, may be of much advantage. Lumbar puncture with with- 
drawal of some of the cerebrospinal fluid has been reported to have 
brought about a cure. 

In the treatment of meningitis I am convinced that time and 
patience, with absolute quiet and the mercurials, will do more than 
harsh or hasty methods. 

SYPHILITIC SPINAL MENINGITIS. SPINAL SYPHILIS. 

Syphilis affects the spinal cord, just as it does the brain, in various 
ways. Certain late products of syphilitic infection, such as the so- 
called parasyphilitic troubles, like locomotor ataxia, will not be dis- 
cussed here. Under the above heading, I will consider rather the 
true syphilitic diseases, namely, meningitis, meningomyelitis, gumma. 

Our knowledge of spinal syphilis is less than our knowledge of 
cerebral syphilis ; nevertheless a sharp distinction should always be 
made, when possible, between syphilitic disease and other affections of 
the cord that may resemble syphilis. 

Etiology. — Constitutional syphilis, acquired or inherited, is of 
course the etiological factor in the production of spinal syphilis. ( )ther 
determining influences are the age of the patient, his mode of life, the 
manner of the primary treatment of the constitutional disease, trau- 
mata, colds and other infectious disease. 

Spinal syphilis usually makes its appearance early, when it does 
occur, after the initial lesion. Nonne detected it as early as three 
months after the acquisition of the syphilis, in most of the cases it 
appears in about a year after, though in some eases it may not develop 
until many years after. In the earlier eases gummatous meningitis 
is the predominant lesion ; in the later eases slow degenerative processes 
and sclerotic conditions arc more frequent. 

Pathology and Pathogenesis. — Huebner enumerates four Min- 
eral forms of spinal syphilis: 

First, neoplasms of syphilitic origin, including single tumors and 
small multiple and disseminated formations on the spinal membranes. 

Second, syphilitic callus, there being found post-mortem a cir- 
cumscribed induration of the cellular tissue about the cord, generall) 
with adhesions of the dura mater. 

Third, simple softening of the cord. This Steenberg describes, 
though Huebner doubts whether it .should be considered a distinct 
syphilitic lesion. He also doubts the existence of a pure syphilitic 
mvelitis. 



520 - THE NON-NEURON IC DISEASES 

Fourth, cases in which symptoms of acute ascending paralysis 
(Landry's paralysis) occur without discoverable post-mortem findings. 

After giving a report of a case which manifested symptoms to 
classify it with Huebner's fourth series, Wood states that he doubts 
whether these cases ought to be regarded as syphilitic at all. Cer- 
tainly his own case, of which it was difficult to obtain a complete 
autopsy, resembled one of peripheral neuritis as much as anything 
else. The cases of Huebner and Kussmaul were not examined for 
lesions of the peripheral nerves, so that the fourth class, as a form of 
syphilis, has scarcely been established. 

In the production of the second and third classes of Huebner, 
syphilitic infiltration and gummatous formations play an important 
role ; so that the softening of the cord and the development of callus 
should be regarded in the light of secondary effects rather than as 
direct syphilitic lesions of the cord. 

This leaves only the first class to be considered. 

Syphilitic neoplasms are generally connected with the spinal mem- 
branes. They may grow inward upon the cord and produce destruc- 
tion of the medullary elements and even chronic inflammation and 
softening; or they may extend outward and cause agglutination of all 
the spinal membranes, pressure of the nerve roots, and even disease 
of the osseous vertebrae. There are probably, therefore, two forms of 
spinal syphilis or gummatous disease — that in which the membranes 
are chiefly the site of the disease (Wood), and that in which there is 
an infiltration of the cord from its own vessels (Rumpf). 

The meningitis is usually of the pia mater and arachnoid, though 
in some instances it has been seen to develop from the inner surface 
of the dura. The membrane is thickened, opaque, clouded and more 
or less bound to the cord and the nerve roots. Granulation tissue is 
formed and over the membranes is spread a gelatinous, fibrous sub- 
stance. The cord is swollen and the dura is held to it by adhesions. 
Yellow, gray, soft or hard deposits are seen scattered here and there 
resembling small, circumscribed tumors. The process is not uniform 
over the whole membrane for in one place it may be highly vascular 
with thick cellular deposits, and in another hard and fibrous in char- 
acter. Usually it is more pronounced in the region of the posterior 
columns, a fact which by comparison lends some color to the theory 
of Redlich and Obersteincr that locomotor ataxia is pathogeneticallv 
primarily a chronic form of posterior spinal syphilitic meningitis. 

In most of the cases the periphery of the cord itself is involved in 
the inflammatory process, so that we have a meningo-myelitis rather 
than a simple meningitis. Sometimes the granulation tissue sends 
septa-like extensions into the cord substance which cause inflammation, 
atrophy, destruction and sclerosis in the adjoining tissues. The nerve- 
roots are usually implicated, though it is possible for them to remain 
normal where they pass through the inflamed and thickened 
membranes. They usually show signs of infiltration and atrophy. 
Spots of softening and old hemorrhagic inflammatory foci are some- 
times present in the cord, having been caused by the obliteration of 
the inflamed and thick-walled bloodvessels. Oppenheim is responsible 



THE NON-NEURONIC DISEASES 52 1 

for the statement that a simple disseminated and diffuse myelitis, a 
poliomyelitis (?) may develop from syphilis. Isolated gummata have 
been reported a number of times, and Kahler has attempted a descrip- 
tion of what he calls a multiple gummatous neuritis of the nerve roots. 

Specific gummatous meningitis, with secondary results, is the 
primary lesion of true spinal syphilis as it is of true cerebral syphilis. 
In fact the separation of brain syphilis from spinal syphilis is a mere 
arbitrary distinction based solely upon a convenient anatomical classi- 
fication of the parts of the nervous apparatus. In a large percentage 
of cases both the brain and the cord are affected together, the brain 
symptoms merely over-shadowing those of the cord. 

Symptoms. — When examining a case of suspected spinal 
syphilis, it is necessary to remember that the lesion may be meningeal, 
producing symptoms similar to those of non-specific spinal meningitis ; 
and that, on the other hand, it may consist of an infiltration of the me- 
dullary substance itself, giving rise to symptoms indicative of destruc- 
tion of the sensory-motor tracts. When the gummatous disease is men- 
ingeal, the earliest symptoms will be those of pain or paresthesia and 
spasm or paresis, due to compression and irritation of the anterior and 
posterior nerve roots. Of course, the sensory symptoms will be re- 
ferred by the patient to the peripheral terminations of the nerves whose 
roots are undergoing irritation. The principal difference between 
gummatous disease of the meninges and simple, non-specific, subacute 
or chronic meningitis, is that the symptoms of the former are apt to be 
more sharply defined or localized than those of the latter. The reason 
for this is obvious, since the former lesion is more in the nature of a 
tumor with comparatively well-defined limits. 

According to Erb,. the symptoms of syphilitic disease of the spinal 
cord closely resemble those of myelitis transversa dorsalis ; but the two 
are, nevertheless, distinguishable by a number of typical signs. The 
walk, posture, and motion are quite characteristic, and simulate those 
of spastic paralysis. The tendon reflexes are apt to be marked, with- 
out much muscular tension. 

The pains, when present, are usually sharp and cutting, and when 
the lesion is located in the dorsal or lumbar region they assume the 
girdle form. Xot unfrequently they resemble the lightning pains 
tabes dorsalis. Rarely are they dull, aching, and continuous. Often 
there is no pain at all. On account of the usual meningitis accom- 
panying the gummatous deposit, there is more or less local tender- 
ness of the spine on pressure. Wood States that in several instances 
this local tenderness was attributable to involvement of the vertebral 
periosteum and vertebrae. All the various sensations common to local 
meningitis are characteristic of this form of spinal syphilis, such a> 
numbness, formication of the extremities, "pins-and-needles" sensa- 
tion, and other bizarre paresthesia? down to the ultimate condition oi 
complete anaesthesia. There is always distinguishable impaired sensi- 
bility, but severe pain is not generally felt, according to the observa- 
tions of Erb. Atrophy is not present. There is little or no invol 
ment of the head and cerebral nerves. Rarely are the muscles of tin- 
eye implicated. There is nothing abnormal psychically. 



522 THE NON-NEURONIC DISEASES 

The motor symptoms are the same as those of localized non- 
specific irritative meningitis, such as rigidity of the neck and limbs, 
tremor, exaggeration of the reflexes, severe cramps excited by move- 
ment. Later on, complete paralysis supervenes. If the palsy increases 
rapidly after long-continued disturbance of sensation, it is almost 
pathognomonic of syphilitic disease, according to Wood. The sphinc- 
ters are generally included in the final symptoms. Bedsores and other 
trophic troubles occur, often with elevated temperature and general 
septicaemia. 

In a case of syphiloma of the cord and cauda equina, reported by 
Osier, death occurred from diffuse central myelitis. There were pains 
in the legs, particularly in the left, which underwent rapid wasting 
and presented vasomotor changes. There were pains in the arms, 
especially the right, without wasting. There was absence of control 
of the bladder and rectum for two months before death. There were 
bedsores and arthritis in the knees and ankles. Toward the close of 
life high fever with delirium came on. There was a gumma in the 
antero-lateral columns of the cervical cord, opposite the right fourth 
anterior nerve root. Gummata also involved the third, fourth and 
fifth anterior sacral nerve roots, and the second and third posterior 
sacral roots on the left side. Many of the symptoms in this case were 
due to the accompanying lesions resulting from the presence of the 
syphilitic new formations. A differential diagnosis in such cases, 
though extremely difficult, is important if at all possible. 

In syphilitic disease of the upper cord there may be diplopia, 
amblyopia, and pupillary irregularity. Tinnitus aurium occurred in a 
case reported by Weber. 

The symptoms of the second form of spinal syphilis, namely, 
syphilitic infiltration of the cord, are usually slower in their onset and 
vary according to the location of the lesion. As the latter is more or 
less diffused, so will the symptoms be more or less indefinite. They 
will range all the way from hyperesthesia to anaesthesia, from spasm 
to paralysis. Spastic paraplegia without much pain is highly indica- 
tive. Sometimes the symptoms closely resemble those of locomotor 
ataxia. True syphilis of the cord does not follow the course of the 
sensory and motor tracts as do the various systematic scleroses and 
subsequent degenerations. The symptoms are, therefore, much more 
mixed and indefinite. 

There is a class of cases, probably included in Huebner's fourth 
class, described by many writers under the title of acute syphilitic 
myelitis, acute syphilitic paraplegia, acute syphilitic spinal paralysis. 
They usually attain their maximum degree of severity in a few hours 
or a few days. They may have prodromal symptoms long before, how- 
ever. Most of these cases subside and pass into a state of partial re- 
covery ; a few mild cases make a complete recovery ; some pass to a 
very rapid fatal termination. The symptoms are all those of a typical 
myelitis. 

There are cases that resemble subacute and chronic myelitis and 
are progressive in character. Erb described a type in which there 
appears a slowly developed spastic paraplegia, exaggeration of the 






THE NON-NEURONIC DISEASES 523 

Itnee-jerks, and disturbance of the bladder. In its pure form there 
are no sensory phenomena. Most of the cases prove to be not of the 
pure type, as sensory and other symptoms appear which link them to 
the great group of variable cases of spinal syphilis. Erb did not there- 
fore describe a type of the disease, but rather a particular symptom 
group. Kuh says that in Erb's spinal paralysis the disease has its origin, 
in all probability, in syphilis of the vessels of the cord in the dorsal re- 
gion, the lesions of the cord being secondary and involving mainly 
the lateral tracts and slightly invading the posterior columns. Kowa- 
lewsky affirms that the cases are quite common in the male sex be- 
tween the ages of thirty and forty-five. With Oppenheim I am in- 
clined to regard these cases of Erb's as merely representing a certain 
stage of the usual form of syphilitic mcningo-myelitis. As Dercum 
well says, ''When we recall the fact that the virus of syphilis expends 
itself mainly upon the membranes and bloodvessels, it is not surprising 
that most varied clinical pictures should present themselves. Xot a 
single symptom can be taken as constant for all cases. Even the 
spastic character of the gait may be lacking. Instead of flaccidity, con- 
tractures may be present and under certain conditions the knee-jerks 
may be absent.'' The same remarks apply to the cases which Oppen- 
heim finds so similar to tabes and which he has denominated syphilitic 
pseudo- tabes. 

A simple gliosis, an amyotrophic lateral sclerosis, and other dis- 
eases have been simulated by syphilis. As in brain syphilis, so here, 
the great diversity of symptoms, their changeability and inconstancy, 
are one of their characteristic features and go a long way toward es- 
tablishing the diagnosis of syphilis in doubtful cases. 

Diagnosis. — There are certain manifestations of spinal syphilis 
that so simulate other affections of the cord, and are in them selves 
so indefinite* and irregular, that a diagnosis is always a matter of ex- 
treme nicety. In such cases a course of anti-syphilitic treatment has 
sometimes been resorted to before any diagnosis could be made. The 
more we can avoid, however, such indirect, empirical methods of 
making diagnoses, and the more we can learn to depend upon the 
direct manifestations of the disease, the better it will be for the patient 
and the more creditable to the science of medicine. 

The diagnosis of spinal syphilis is best made by the exclusion of 
other spinal affections and by remembering that any one of these other 
affections, associated with a history of syphilis and presenting more or 
less unusual manifestations, is very apt to be syphilitic in origin. If a 
case of apparent locomotor ataxia, for instance, shows an absence of the 
usual fulgurating pains, or the presence of the patellar reflex, spinal 
syphilis rather than posterior spinal sclerosis should at once be 
thought of. 

Simple myelitis, compression myelitis, multiple sclerosis and (lis 
ease of the lateral and posterior tracts, may all be simulated b) syphilis. 
Hence the differential diagnosis ran be taken up better under th 
various heads. 

Prognosis. — The prognosis of spinal syphilis should always 
guarded, even though great improvement is obtained sometimes by 



524 THE NON-NEURONIC DISEASES 

appropriate medication. Occasionally absolute cures have been made 
More often, however, the delicate constituents of the cord have been 
irreparably damaged when the case first comes under observation, and 
then only a prevention of further injury can be hoped for. 

The less the cord itself is involved the better the prognosis. When, 
paralysis has continued several months no improvement can be ex- 
pected. Spastic paresis, bladder trouble, etc., will continue. Relapses 
are always liable. 

Treatment. — The treatment usually resolves itself into the ad- 
ministration of mercury and the iodides. The object is to neutralize at 
once the syphilitic poison, to sustain the vitality of the cellular struc- 
tures, and to remove as quickly as possible any gummatous enlarge- 
ments that may be exerting a deleterious pressure. Each case is a. 
law unto itself, but in all cases bold, heroic 'treatment is usually needed 
to check at once all further damage of the nervous elements. Hot and 
cold spinal douches, suspension, massage, all have their applicability 
in appropriate cases. The indications are the same as in any of the 
various forms of organic disease of the spine. Spinal syphilis should 
be managed just as any other disease of the cord and its membranes, 
plus the administration, heroically and for a long period of time, of 
the requisite antisyphilitic remedies. The administration of these is 
the same as for brain syphilis, to which section the reader is referred 
for more detailed discussion. 

SPINAL MENINGEAL HEMORRHAGE. 

Hematorrhachis. — This condition is so commonly secondary to- 
some injury or other disease that some authors do not speak of it at 
all as a special affection. It does occur, very rarely, however, as a 
primary trouble. Its symptoms are slightly characteristic' I deem it 
worthy of special, brief consideration therefore. 

Etiology. — The hemorrhage may occur outside of the dura mater 
(extra-dural, extra-meningeal hemorrhage), or it may take place be- 
tween the dura and the cord (sub-dural, intra-meningeal hemorrhage). 
The former is the result of traumata, blows, falls, fractures, disloca- 
tions and disease of the vertebrae. The rupture of an aneurism may be 
the source of the hemorrhage. The blood springs usually from the 
great venous plexuses that surround the dura. 

Sub-dural hemorrhage may result from the same causes as the 
extra-dural, and from all the causes enumerated under the head of 
hematomyelia in a following section. The clot may extend only 
an inch or so and not compress the cord at all. On the other hand it 
may reach the entire length of the canal and exert very severe pres- 
sure upon the cord. Most of these hemorrhages occur from the pial" 
vessels in the cervical region. While blood may pass up even into the 
ventricles of the brain, or vice versa, one must be on his guard in as- 
suming this, for the intra-cranial and intra-spinal hemorrhage under 
such circumstances are more apt to be simultaneous phenomena.. 

SYMPTOMS. — The symptoms of hematorrhachis are characteris- 
tically meningitic, that is progressively irritative and paralytic upon 



THE NON-NEURONIC DISEASES 525 

the spinal cord and spinal-root functions. The suddenness of these 
-symptoms and their appearance at first without fever indicate their 
hemorrhagic origin. Preceding them there may be slight premonitory 
manifestations and in a few days after their appearance all the signs 
of a meningitis exhibit themselves. There is pain in the back and pains 
shooting along the course of the spinal nerves. The nerve pains are 
neuralgic in character and remittent or intermitttent. The nerves them- 
selves are not locally tender as they are with the pains of neuritis. 
The spine is very tender, however. The cranial nerves and head and 
mind are all unaffected. The skin is generally hyper&sthetic, and there 
are usually various paresthesia such as tingling, pins-and-needles sen- 
sation and numbness. The muscles are spasmodic in the same areas as 
the sensory phenomena. Soon they become rigid and contracted. The 
back is arched in opisthotonos. Finally in some cases the condition 
goes on to almost, but not quite, complete anaesthesia and paralysis, es- 
pecially in the lower limbs. Later on and toward the close trophic 
manifestations appear and even signs of a distinct me ningo -myelitis. 

According to the location of the hemorrhage so will the clinical 
picture be slightly altered. If it occurs in the lumbar region the pains 
are felt entirely in the legs. The sphincters are paralysed. Paraplegia 
■comes on early and the patella reflexes are lost. Sexual irritation may 
be a troublesome symptom in the beginning. Dorsal hemorrhage sends 
the pains shooting around the chest and abdomen. When the 
seat of the trouble is the cervical enlargement, the pains are felt in 
the neck and arms. Later on the paralysis is spastic in the lower and 
flaccid in the upper extremities though this is rare and only in very 
advanced cases with considerable involvement of the cord. The neck 
may be rigid and immovable. Swallowing is difficult. Respiration is 
disturbed. The pupils are dilated. 

Diagnosis. — The history of an injury or appropriate cause for 
a hemorrhage, the onset of irritative, non-febrile symptoms of a men- 
ingeal character, ought to go far towards making the diagnosis easy. 
Meningitis itself approaches more slowly and insidiously, and is ac- 
companied by fever, and symptoms that tend rather to continuously 
progress and not to recede, as they often do in hemorrhage. In mye- 
litis there is fever, more marked paralysis and anaesthesia and not tin- 
distinctive irritative signs of meningeal trouble. 

After all, however, it must be admitted that there is such a dose 
relationship between all of these troubles, hemorrhage, meningitis and 
myelitis, that a differential diagnosis is sometimes, and under certain 
conditions, peculiarly difficult and even impossible. At all time 
can hardly amount to more than a strong suspicion, so frequently and 
generally do all three diseases overlap and run into one another. 

Prognosis. — Most of the severe cases prove fatal in a few hours. 
•Others recede somewhat symptomatically, then become a meningitis 
and so run their course. If after a few days, three or four, the cord 
manifests no signs of implication, recovery may be hoped for. I 
vical hemorrhage for obvious reasons is more dangerous than hem 
orrhage elsewhere in the spine. Traumatic and infection- iften 

recover. What is called typhoid spine is sometimes a slight hemor 



526 



THE NON-NEURONIC DISEASES 



rhagic meningitis or meningo-myelitis. I have seen such cases recover 
after one or two years. 

The cause of the hemorrhage, its extent, its volume, the course 
and severity of the secondary meningo-myelitic phenomena will all 
determine the prognosis. 

Treatment. — This is about the same as that recommended for 
hematomyelia. The posture should be prone on the stomach or side, 
and absolute quiet should be maintained. To obtain this sedatives will 
have to be rather freely given to ease the pain. The bowels should 
be freely moved. Leeches may be applied to the anus, or cups to the 
spine. The ice bag to the spine is a regulation measure. In robust 
cases, venesection may be employed. Aconite and ergot cannot do 
much harm if judiciously used, but unfortunately they will do very 
little good. In purpura Dana recommends the trial of the mineral 
acids or chloride of calcium. The meningitis and residual phenomena 
are to be treated on general principles laid down for them elsewhere. 
Mild persistent counter-irritation to the spine and the steady use of 
small doses of mercury for a long time have helped me much in the 
later management of these cases 

DISEASES OF THE SPINAL CORD. 



CIRCULATORY DISEASES. 



The arrangement of the bloodvessels in and about the spinal cord 
is such that temporary changes in them are not liable to occur, and 
permanent changes are the result of disease and not of mere func- 
tional derangement. Hence, as before mentioned, ancemia and hypere- 
mia of the cord are unknown except under very special circumstances. 
What is seen in this respect after death is absolutely no criterion as 
to what is present during life. In fact if all hypotheses were to be 
discarded, all analogies cast aside, all logical deductions waived, and 
we were to depend absolutely and entirely upon what the cord reveals 
post-mortem, we would probably say that anaemia and hyperemia never 
occur. Such is the position taken by some of the more radical pathol- 
ogists. They declare that the few changes that are observed in the 
bloodvessels and related tissues are due to gravitation, lethal changes 
observed in all fatal diseases, and from various mechanical causes oper- 
ating upon the corpse ; and that the elaborate symptoms so often noted 
during life and attributed to the alteration in the amount of blood in 
the cord, are really due to other factors such as toxaemia, quality of 
the blood, pressure and velocity of the flow. More conservative au- 
thorities still hold that anaemia and hyperaemia of the cord may and 
do occur, but arc rare and are little comprehended by us. The symp- 
toms that have been so elaborately described by the older authors, 
cannot for a surety be assigned to conditions about which we know 
so little and whose very existence is problematical. 



THE XOX-XEUROXIC DISEASES 52/ 

ANAEMIA. 

As a simple, primary condition, temporary or permanent, we 
know absolutely nothing with certainty about anaemia of the spinal 
cord. There are some experimental observations and clinical facts 
that are highly suggestive, but the conclusions that are drawn from 
them must not be regarded as the incontrovertible actualities. For in- 
stance it is an interesting fact, and one that leads to the drawing of 
suggestive comparisons, that the ligation of the aorta was, in a few 
moments, followed in the experiments of Herter, by complete para- 
plegia and paralysis of the sphincters. Clinically paraplegia has been 
seen to follow either immediately or at the end of a few days, pro- 
fuse hemorrhages from the stomach and uterus. The degenerative 
changes in the spinal cord in pernicious anaemia are well recognized. 
As a part of a general anaemia, chlorosis and debilitated blood state, 
the spinal cord may readily be supposed to suffer implication. As a 
sequel to profuse hemorrhage, exhausting diarrhoea, and mechanical 
obstruction of any sort which shuts off its blood supply, the anaemia 
of the cord may be frankly admitted as a possibility. Even local 
anaemia must undoubtedly exist in cases where the local circulation is 
affected by a tumor or other cause of obstruction. 

When, however, we attribute to anaemia zveakncss of the legs, 
pains in the back, various parcesthesicc, such as numbness and tingling, 
we are reasoning beyond the proofs, for these symptoms may be due 
to special changes in the nervous elements rather than to the alteration 
in the blood quantity, or they may be toxaemic in origin, or they may 
be a part of the general symptom-complex of the general or local 
disease with which the anaemia is associated. 

HYPEREMIA. 

Of this some writers think we have a little more definite knowl- 
edge than we have of anaemia, and they even discuss the condition 
elaborately under the heads of etiology, pathology, symptoms and treat- 
ment. It seems to me that in the present state of our knowledge such 
an elaboration of the subject is unwarrantable. Much of what is said 
cannot be denied, to be sure, but very little of it can be supported with 
positive proof. As Gowers well says, "volumes might be filled by the 
collected descriptions of the varieties and symptoms of congestion ^i 
the spinal cord — descriptions in which the unrestricted play of 'scien 
tine' fancy has elaborated a symptomatology for the separate eon. 
tion of every part of the spinal cord." 

As a condition in the beginning of myelitis it is undeniable. It is 
not impossible that it may occur in excessive coitus, in certain forms 
of violent exercise, in suppressed menstruation, in strychnine poison 
ing, as a residuum of a meningitis or trauma, as a part of the general 
symptom-complex of some other disease. \s I say, it IS not impossible 
that such is the case, but where and what are the proofs? Tin- symp- 
toms do not confirm it. The reputed heaviness and weight in the 
limbs, the numbness, the creeping sensations, the neuralgic pains, the 



528 THE NON-NEURONIC DISEASES 

weakness in the legs, the muscular twite kings, the disturbances of the 
sphincters, the general tendency to paraplegic phenomena, the very 
doubtful increase of distress when a posture on the back is assumed, 
may all be due to anaemia, to circulatory disturbances in the meninges, 
to beginning or transient inflammatory states, to irritative lesions of 
various sorts, to nutritional disturbances in the nervous cells or even 
to other conditions in the blood itself, than to the mere excess of its 
quantity. No, it will not do to assume a hyperaemic pathology on such 
a diffuse, indefinite, loose basis as this symptomatology appears to be. 
Pathology and treatment suggest no proof. It is singular how au- 
thors recommend in one paragraph the use of counter-irritation, cup- 
ping and the ice bag to the spine, morphine and bromides internally 
and in the chronic cases ergot, muriate of ammonium, iodide of 
potassium and the galvanic current, when in the paragraph almost 
immediately preceding it was admitted that these symptoms may be 
due to very different conditions from that of congestion and that the 
simple existence of congestion is open to doubt. If the presence of 
another disease can be made out, we may be at liberty to suppose that 
this therapy affects that disease and so modifies the spinal manifes- 
tations. In some cases the beneficial results may be partly psychic in 
character. I have often in hystero-neur asthenic cases obtained the 
happiest kind of psychic effects from the use of vigorous cupping of 
the spine. In such cases it is a favorite trick to get the patient's 
thoughts in regard to her spine runing in another direction by the use 
of cups, galvanism, etc. And I have thus relieved many symptoms 
similar to those above but I did not fancy I was curing a spinal con- 
gestion. In fact I am still of the opinion that the treatment and its 
good results were alike largely psychic. 

EMBOLISM. THROMBOSIS. ENDARTERITIS. 

These conditions are comparatively rare in the spinal cord. 
Thrombosis of the minor vessels, together with endarteritis, undoubt- 
edly underlies some of the acute and chronic focal diseases of the 
cord, or may be an associative or complicating feature in the pathology 
of these diseases. As a part of general senile changes and senile 
pathology, endarteritis may be seen quite frequently in persons past 
middle life. It is not, however, a special cord condition but the arteries 
of the cord are affected like those in the rest of the body. Thus in 
younger persons there is a special as well as a general syphilitic 
nodular periarteritis or endarteritis, possibly with gummatous menin- 
gitis. Arteritis obliterans and miliary aneurism may be seen biit they 
are far rarer in the cord than they are in the brain. 

SPINAL HEMORRHAGE. 

Hematoniyclia. Hemorrhage into the Spinal Cord. — As a primary 
condition, hemorrhage into the substance of the cord is exceedingly rare, 
even being denied by some. It is thus in marked contrast to hemorrhage 
into the brain, the difference being probably due to the longer course 



THE NON- NEURONIC DISEASES 52<) 

of the spinal bloodvessels. As a secondary condition, associated with 
myelitis, tumors and cavities, or capillary hemorrhages generally in se- 
vere tonic and clonic spasms, hemaiomyelia is of little clinical interest 
because its symptoms are so masked by those of the primary disease, 
that the diagnosis is always uncertain. 

Many descriptions have clearly been based upon the secondary 
forms of the trouble. I will discuss here only the primary form. 

Etiology. — Men are more subject to it than women. It occurs 
most often in middle adult life. It has been seen in infants. Alcohol- 
ism, degenerated arteries in the aged, the hemorrhagic diathesis, pur- 
pura and other factors doubtless may predispose to it. The influence 
of heredity, except through the circulatory apparatus, is nil, and cer- 
tainly not what it is in cerebral apoplexy. 

Bv all odds, some form of trauma is the leading cause of spinal 
apoplexy. Blows upon the spine, falls, strains, wrenches, lifting of 
heavy weights, excessive exercise produce probably nine-tenths of 
the cases. Somewhat traumatic in a way are those cases said to have 
"been due to excessive coitus, exposure, suppressed menstruation, bleed- 
ing piles, difficult parturition. The cases due to fractures of the spine, 
dislocations, inflammations, syphilis, neoplasms, cavities, tetanus and 
convulsions are of course merely secondary and of very little practical 
interest. 

Pathology and Pathogenesis. — The central vessels of the cord, 
supplying especially the gray matter are the chief sources of the hem- 
orrhage. Miliary aneurisms are exceedingly rare upon them. Their 
coats of course may be degenerated as the result of disease or age. 
Generally, however, in the primary form of the trouble, there is no 
very great change observable in them. After the rupture takes place 
the blood pours out into the surrounding gray substance extending up 
and down the cord and into the horns, especially the posterior. The 
white matter is not usually implicated, certainly not to any very great 
extent. It is more generally compressed than directly damaged. Mye- 
litis of course soon lights up in and around the hemorrhagic focus, 
the tissues become softened, disappear and leave a cavity in a few 
cases. This process Van Giessen calls heniatomyelo porosis, to dis- 
tinguish it from hematomyelia. Sometimes the clot may be so 1 arm- 
that the white substance of the cord forms a mere thin, ragged wall 
around it. It may lacerate its way through the white matter and ex- 
tend beneath the meninges. The cord is usually enlarged, softened 
and ruddier in hue near the extravasation. In small hemorrhages there 
may be no noticeable external changes. 

Symptoms. — The first great characteristics to be always noticed 
about the symptoms are that they appear suddenly and are accom- 
panied by febrile phenomena. As time passes, however, fever, pos 
sibly some slight recession of the symptoms or the appearance 
others indicates that the secondary myelitis has begun. As the erup 
tion of blood produces a sudden break in the continuity of the cord, 
all parts of the body below it are functionally paralyzed. The patient 
falls, therefore, with a complete paraplegia. This may involve only 
his arms or legs or all four extremities. . liucthesia accompanies it an 1 



53Q 



THE NON-NEURONIC DISEASES 



the sphincters lose their control. In some cases there are slight pre- 
monitory weakness, tingling and numbness for a few moments, then 
the shock comes as just described and is profound all at once or in- 
creases still more than it was at first. At first the reflexes are abol- 
ished but they soon return and in a little while become highly exag- 
gerated. The patient's consciousness and sensorium are unaffected 
and he often complains of pain in the back. 

The site and size of the clot of course may vary and thus greatly 
modify this clinical picture in different cases. The paraplegia indi- 
cates a dorsal or lumbar lesion when it is limited to the legs. In such 
a case the reflexes may remain lost, the sexual functions be damaged 
and the bladder and bowels be involuntarily evacuated. There may 
be a girdle pain, especially when inflammation lights up. A quadri- 

FIGURE 112. 




Cross-section of the spinal cord in heniatomyelia. Hemorrhage into the left 
anterior and posterior horns. (After Minor and Oppenheim.) 

plegia indicates a cervical hemorrhage. Here an atrophic paralysis 
occurs in the arms and a spastic condition in the legs. Unlike lumbar 
hemorrhage, the patella reflexes are now exaggerated. Oculo-pupil- 
lary symptoms occur if the lower cervical region is implicated. 

A unilateral hemorrhage may cause the Brown-Sequard syndrome, 
typical in this case of limitation of the lesion to the gray matter. ( )n 
one side, the side of the lesion, the leg exhibits a spastic paralysis, 
while the arm manifests a partial, flaccid, atrophic paralysis. On the 
opposite side appear anaesthesia, analgesia and thermansesthesia. There 
may be some hvp.esthesia on the side affected with the motor paraly- 
sis. In a few days the case assumes all the characteristics of a typical 
myelitis and the symptomatology of the hemorrhage sinks into that of 
this disease. 

Diagnosis. — The abruptness and paraplegic character of the on- 
set of the trouble should be carefully noticed. There is no fever and 
the symptoms tend to recede a little for a few days when a change 
takes place and the case assumes a myelitic complexion entirely. It is 



THE NON-NEURONIC DISEASES 53 1 

difficult, however, in some cases to distinguish the hemorrhagic from 
the myelitic manifestations. Fortunately the differentiation is rarely a 
matter of any consequence as hemorrhage almost always sooner or 
later develops inflammation in the cord and in myelitis hemorrhage 
may or may not occur without the progress of the disease being very 
materially affected. 

Poliomyelitis is to be distinguished by the febrile symptoms and 
the symptoms that indicate especially damage to the anterior horns. 

Hemorrhage into the spinal membranes is different from hema- 
tomyelia clinically in that there is pain in the back, pains of a radiat- 
ing character along the course of the spinal nerves, rigidity, spinal- 
root signs and other indications of meningeal irritation. Some have 
employed and recommended spinal puncture to positively diagnose 
hematorrhachis. One would fear an increase or renewal of the hem- 
orrhage in some cases from the disturbance of the cerebrospinal pres- 
sure in such a manoeuvre. 

Prognosis. — This is always serious for if death does not occur 
early, it will in all likelihood later, from the myelitis. Only large hem- 
orrhages destroy life early. Improvement often occurs and occasionally 
complete recovery has happened. A small hemorrhage in the dorsal 
region holds out the best chances for recovery. When myelitis de- 
velops, the prognosis depends upon that. If sensation returns early 
the outlook is hopeful. Early trophic manifestations are discouraging. 
Some cases recover with permanent muscular atrophy and degenera- 
tive reactions. 

In a word, the size of the hemorrhage, the extent and location of 
the clot and the onset and severity of the subsequent myelitis must 
all be carefully taken into account in affirming the prognosis. 

Treatment. — Absolute rest in bed for the first few days and 
weeks must be enjoined. The patient should lie on his side or abdo- 
men. Ice should be applied over the seat of the hemorrhage, or as near 
it as possible. Aconite in small doses may be given to restrain the 
heart action. Ergot by the mouth in a few large doses, or ergotin 
hypodermically have been recommended. Their efficacy is doubtful, 
however. Blood letting is a more powerful measure. 

The later treatment is the same as that for myelitis. 

MYELITIS. 

Myelitis is inflammation of the spinal cord. It may be acute. 
subacute or chronic. It may occur in any part of the cord. As the 
clinical picture of the disease undergoes some variations in accordance 
with the character and location of the lesion, subvarieties of myelitis 
are described, some of which are of sufficient importance to be given 
a special chapter. 

When the inflammation surrounds the edge of the cord it is known 
as peripheral myelitis, or meningomyelitis, since it is usually associated 
with meningitis. When it is confined to the gray matter immediately 
encompassing the central canal it i a periependymal 

myelitis. When it is confined to the gray matter of the cord it is 



532 



THE NON-NEURONIC DISEASES 



known as poliomyelitis. Some authors regard acute anterior poliomyeli- 
tis as a systemic disease because it is limited to the column of gray 
matter that makes up the anterior cornua. "When the disease extends 
completely across the cord it is a complete transverse myelitis; when 
only part way across it is an incomplete transverse mvelitis. These 
forms may all be more or less limited to the cervical, dorsal or lumbar 
regions. Disseminated myelitis shows the inflammation scattered in 
foci irregularly throughout the cord. 

All of these forms, except the anterior poliomyelitis, will be dis- 
cussed in detail under the head of symptomatology. 

Etiology. — Nearly all inflammations of the spinal cord are caused 
by traumatism or infection. Blows upon the back, fractures or dis- 
locations of the vertebrae, stab wounds and wrenchings of the spine 
are among the former ; acute infectious diseases like varicella, sepsis, 
hydrophobia, tuberculosis, syphilis, malaria, etc., are among the latter. 
Gonorrhoea produces it and it may occur in pregnancy and in the puer- 
perium. It has followed tonsillitis, dysentery, erysipelas, typhoid 
fever, pneumonia, cystitis, influenza, tetanus and phlegmonous parony- 
chia. 

Primary acute myelitis is exceedingly rare. The disease may oc- 
casionally occur, however, as a primary infection. The micro-organ- 
isms are numerous, therefore, that enter into the etiology. Among them 
are the streptococci, staphylococci, pncitmococci, diplococci and many 
others. Whether the germs themselves or their toxines are the direct 
cause of the inflammation is still unsettled. The germs are not often 
found in the cord, but this fact does not argue against their being 
the direct cause, for it is a well known fact that they disintegrate and 
vanish as soon as they have accomplished their deleterious work. Op- 
penheim and Grasset believe that myelitis really results from a mixed 
or secondary infection. 

An ascending neuritis has been charged as a cause of myelitis. It 
certainly has followed certain diseases of the urinary apparatus, caisson 
disease and arteriosclerosis. Some of the so-called re-Hex paralyses fall 
in here. 

Among the intoxicants found to have caused myelitis may be noted 
carbon dioxide, carbon disulphide, illuminating gas, chloroform and 
nitrobenzine. 

Adults of early middle life and of the male sex are chiefly affected. 
Dana affirms that over one-half of the non-traumatic and non-tuber- 
culous cases in adult life are due to syphilis. We no longer lay any 
stress upon cold, exposure, over-exertion, sexual excesses or violent 
emotions in the etiology of the disease, except as general predisposing 
factors. 

Pathology and Pathogenesis. — As myelitis is primarily a pure 
inflammation there is at first hypenemia, congestion, enlargement and 
proliferation of the bloodvessels, extravasation of the corpuscles, 
swelling of the perivascular spaces with fluid and a general softening 
and obliteration of the normal appearances. Sometimes the cord is so 
softened that it flows out when the pia is cut. This extreme fluidity 
is partly a post-mortem change. In the early stage the softened area 



THE XOX-XEUROXIC DISEASES 



533 




FIGURE 113. 




-- FIGURE 114. 




FIGURE 115 



Forms of myelitis. Figure 113. Toxic acute column-form. Figure 114. Chronic 
myelitis of the dorsal cord. Figure 115. "Compression myelitis," du< 

cinoma of the third dorsal vertebra. (After Jakob. > 



534 THE NON-NEURONIC DISEASES 

is reddish ; then as the coloring matter of the extravasated corpuscles 
breaks down the softened area becomes mottled, brownish or grayish- 
yellow in appearance; and finally with the gradual absorption of these 
coloring matters it becomes paler and whiter. The term softening 
applied to these three stages of the process should not be confounded 
with the softening, or myelomalacia from embolic or thrombotic 
obstruction. Under the microscope the nervous elements are seen to 
be most seriously damaged. The axis-cylinders and cellular elements 
are swollen, which at first causes a puffing up of the cord and ah 
obliteration of the distinction and line of demarkation between the gray 
and White substance. As degeneration proceeds in these elements the 
cord appears yellowish, smaller and even cystic at times. Granular 
cells are found in abundance, and with the fat drops resulting from the 
breaking down of the myelin are here and there heaped up. The 
neuroglia is proliferated and the spider-like cells of Deiters are numer- 
ous and prominent. In a transverse myelitis this condition of the cord 
extends about an inch or two, shading off above and below. Usually 
the pia mater is somewhat thickened over the diseased area and often 
the whole cord. In severe and secondary cases the cord is often reduced 
in size, rather hard to the touch and under the microscope shows little 
but an excess of connective tissue. In the cases less severe, or the 
parts of the cord less seriously affected, congestion and vascular irri- 
tation are noticeable, some nerve fibres are intact or partially disinte- 
grated, and cells in various stages of degeneration are seen. A good 
deal of amorphous material is present studded with nuclei. 

Symptoms. — In describing the symptoms of myelitis, the trans- 
verse dorsal type is taken as the model and the variations from that 
noted in other types. There are no prodromata in the true sense of 
the word. When the first symptoms make their appearance, the dis- 
ease has already begun its regular course. These early symptoms may 
be of a very fugitive and indefinite character and may come on prompt- 
ly after an injury or they may be delayed and announce themselves 
later in a severe and definite manner. For some time after a strain, I 
have seen the pains diagnosed as rheumatism and the attending physi- 
cian chagrined to observe all the signs of a transverse myelitis, with a 
fatal issue, follow. I have seen in consultation a case in which a mere 
disturbance of the bladder with slight, fugitive pains as the only trouble 
that sent the patient to his doctor. 

It is well to be alert when such indefinite, slight, changeable sensory 
phenomena, with motor weakness, are complained of in the history of 
syphilis or after an injury, for in many cases they will be seen to be 
the early manifestations of a genuine myelitis. 

In the larger number of cases the symptoms appear rather abruptly, 
and in a few hours or a few days rapidly rise to their height. There 
is an initial numbness in the legs, beginning in the feet. Pains of a 
dull, aching character are complained of in the back, around the lower 
part of the body and even down the legs. The legs feel heavy and 
weak. The patient notices that his walking is growing stiff and labored. 
The numbness graduall) increases in area and passes into a condition 
of anaesthesia. The upper limit of the anaesthesia, usually near the 



THE NON-NEURON1C DISEASES 535 

level of the umbilicus, is fairly well marked. Xear this point is felt a 
cincture pain or constriction girdle sensation. Sometimes for an inch 
or two above this the skin is hypercesthctic. The bowels are constipated 
and there is some incontinence of urine. The temperature may be 
elevated a degree or two but never as much as in meningitis. By this 
time the disease has assumed its typical clinical appearance, the symp- 
toms of which are so characteristic that they call for a little more detail 
of description. 

The most obvious symptom of a fully developed attack of myelitis 
is paraplegia. This paralysis is a true paralysis, spastic in character, 
and affects all of the muscles of both legs. Both the immobility and 
spasticity are of course due to the break in the continuity of the cord 
and the separation of the brain from the lower motor neurones of the 
lumbar area. The myotatic irritability of the muscles of the legs, as 
well as the tendon reflexes, are greatly exaggerated. A slight tap causes 
them to contract violently and when this is observed in conjunction 
with the profound ancesthesia, the symptom is most impressive. The 
limbs at first lie extended but as the rigidity of the muscles increases, 
contractures come on and they become strongly flexed at all of the 
joints. On this account the patient lies on his back or side with his 
legs drawn tightly up towards his belly. Often there are twitchings 
and jerkings and other spontaneous movements in the legs, of which 
the patient is perfectly unconscious except as he happens to see them. 

As a rule all forms of sensation are lost in the legs and lower part 
of the body. This ancesthesia is complete and its upper limit is clearly 
defined by a ring around the body. At a point above this upper border 
of the anaesthesia there is a girdle or constriction band which at first 
may be painful but which later on becomes a feeling of pressure or of a 
vise-like band. For some little distance above the girdle-pain and 
around the body the skin is hyperaesthetic. As this anccsthetic border 
with its hxpercesthctic area above moves up or down with the exten- 
sion of the lesion, it enables one to make a fairly accurate localization 
diagnosis of the site and probable extent of the lesion. 

When the anaesthesia is not complete it is most marked in the 
sense of touch, less so in that of temperature, and least of all in that oipain 
The anaesthesia involves the bladder and rectum. On account of this 
and the paralysis of the sphincters, the functions of the bladder and 
rectum cannot be controlled by the patient. Incontinence and reten- 
tion of urine and faces are most significant symptoms of this form of 
myelitis. Priapism occurs as well as sexual impotence. 

Bedsores in most cases begin to develop early. These are genuine 
trophic symptoms, though of course they are favored, by weight and 
pressure, loss of sensation and consequent uncleanliness. M<>- - 
these sores occur over the trochanters, the sacrum or in the toes, and 
sometimes they burrow so deep as to expose tin- underlying b 
Pyogenic infection plays a role also in their production. Pemphigus 
and other trophic skin troubles sometimes occur. 

Among the vasomotor and secretory disturbances are tin- arthro- 
pathies, cedema and anidrosis. The -kin is rough and cold and con 
gested. Sometimes excessive perspiration occurs. 



536 



THE NON-NEURONIC DISEASES 



There is no muscular atrophy nor electrical change. 

In a word the cardinal symptoms of the typical form of myelitis, 
namely, the transverse dorsal, are spastic paraplegia, anaesthesia, exag- 
geration of the superficial and deep reflexes, cincture-pain, disturb- 
ance of the vesical and rectal sphincters, bedsores and other trophic 
manifestations, and certain vasomotor and secretory symptoms. A 
few words must now be devoted to the changes in the above clinical 
picture caused by a change in the location of the lesion. When the 
latter does not extend completely across the cord, all of the usual symp- 
toms are less complete. For instance, the paraplegia is more of a paresis 
and is irregularly distributed. The same is true of the anaesthesia and 
the trophic symptoms. The symptoms may even be unilateral or they 
may be more pronounced on one side than on the other. In some rare 
cases Brown-Sequard's phenomenon is present, namely, paralysis on 
the side of the lesion with anaesthesia on the opposite side. The 
lesion, moreover, may extend up and down the whole dorsal, or in- 
volve a part of the dorsal with the lumbar region. It may be completely 
or incompletely transverse. The symptoms under these circumstances 
will be slightly modified but in a way that can be easily imagined. In 
the main they will represent the general picture, but the reflexes will 
be abolished, the paralysis will be more profound and the atrophy will 
be more distinct. According to Bastian, when the lesion is such that 
there is a total destruction of the conducting tracts above the reflex- 
arc, that reflex will be decreased or annulled, whereas in a partial or 
incomplete destruction it will be exaggerated. This is not entirely 
proved, however. When the disease is of a slowly progressive charac- 
ter, the reflex functions of the cord may be retained and the muscular 
tone may remain unimpaired, thus modifying Bastian's hypothesis to a 
certain extent. In compression of the cord, where the anatomical 
lesion is slight or incomplete, there may be a physiological loss of 
function, and the same may be true of the functions of the cord below 
a transverse lesion. At all events, as Warrington has pointed out, 
no case of incomplete division of the cord has been recorded in which 
all the symptoms described by Bastian were present, and in which the 
lumbar enlargement was intact. It was Van Gehuchten who taught 
that the reflexes depend upon the tone of the motor ganglion cells, as 
well as upon the integrity of the reflex-arc, and that therefore the 
reflex may be annulled by a complete destruction of conduction in the 
spinal cord, and exaggerated by a degeneration of the pyramidal tracts. 
This may explain in part the exaggeration of the knee-jerks in some 
cases of transverse myelitis, particularly the slowly progressing or high 
dorsal cases, and its abolition in some other cases, such as the severe 
and complete cases of the lower dorsal or dorso^-lumbar type. 

When the disease is entirely of the lumbar or lumbosacral type, 
the paralysis and anaesthesia are profound, the reflexes are lost, and 
the implication of the bladder and rectum is decided. The paralysis 
is of the flaccid type with atrophy and the reaction of degeneration. 
There are shooting pains in the legs but no girdle sensation about the 
body. Priapism followed by loss of the sexual function occurs. 

A cervical myelitis involves all four extremities, quadriplegia or 



THE NON-NEURONIC DISEASES 537 

paraplegia, and trunk in the paralysis and anaesthesia. When the lesion 
is in the lower part of the cervical cord the paraplegia is spastic in the 
legs and atrophic in the arms. Moreover there are oculo-pupillary 
symptoms from implication of the ciliospinal center. When it is in the 
upper cervical region the arms as well as the legs are spastic and 
paraplegic. Encroachment of the lesion upon the phrenic center causes 
a disturbance in the action of the diaphragm. Sometimes in these high 
forms of myelitis, there are medullary symptoms such as cardiac and 
respiratory disturbances. 

In a central or periependymal myelitis the symptoms bear a re- 
mote resemblance to those of syringomyelia, namely, muscular localized 
atrophy, disturbance of pain and temperature sense with preservation 
of tactile sense, and symptoms referable to the viscera especially and 
vasomotor and secretory apparatus. There may be some pain and 
irritation but they are distinctly less than in the other forms of mye- 
litis. 

Compression myelitis of the periphery of the cord, is characterized 
particularly by irritative symptoms involving the spinal nerve roots. 
It is slow in onset and usually being but a part of a meningomyelitis 
it reveals meningitic symptoms in addition to the myelitic. Therefore 
it is accompanied by muscular twitchings, spasms and contractures, 
sharp pains along the course of the nerves, incomplete anaesthesia and 
paralysis, late involvement only of the sphincters and slight trophic 
manifestations. The reflexes, however, are exaggerated and sooner 
or later there is a spastic paraplegia. 

A disseminated myelitis involving the cord, medulla, pons and 
brain is the type that follows as a rule the infectious fevers. These 
cases are not entirely unlike multiple sclerosis in their symptomatol 
The motor, sensory and trophic symptoms bear the same general char- 
acteristics noted under the head of the latter disease, and depend upon 
the extent and location of the foci of disease. 

Diagnosis. — The diagnosis of myelitis is not difficult in the typical 
cases. It is the modified and complicated forms that give the most 
trouble in this respect. In making a diagnosis special attention must 
be given to the history of the case, its mode of onset and progT 
the distribution of the individual symptoms and the total clinical pic- 
ture that is presented. It is well, as a rule, to keep in mind the cardinal 
symptoms of a typical transverse dorsal myelitis, and with this general 
clinical picture as a sort of schema, to assign the aberrant symptoms 
that may appear with, or in place of, the symptoms of this schema 
to the possible changes in location of the inflammator) Focus. 

Most of the cases of myelitis begin abruptly and attain their climax 
rapidly. Paraplegia, anaesthesia, altered reflexes, disturbed function 
of the bladder and rectum, decubitus, and other trophic, vasi motor and 
secretory manifestations soon announce themselves in all their com- 
pleteness. There may be a chill with considerable elevation of tem- 
perature. Pain is comparatively slight in these acute cases. I 
frequently the cases are subacute and rarely they are chronic. M 
of the chronic cases turn out to be multiple sclerosis with predominat- 
ing spinal symptoms. 



538 



THE NON-NEURONIC DISEASES 



From progressive muscular atrophy and amyotrophic lateral 
sclerosis, this disease can be readily distinguished by its febrile symp- 
toms, its rapid onset and course, its more prominent sensory mani- 
festations, its involvement of the sphincters and its lesser degree of 
muscular atrophy. Spinal tumor is sometimes accompanied by a focal 
myelitis. It is characterized by slow onset, unilateral symptoms not 
unfrequemtly of the Brown-Sequard type, and signs of spinal nerve 
root irritation and compression. The metastatic origin of the neoplasm 
can sometimes be made out and in some cases it can be definitely 
localized. In locomotor ataxia there is no true paralysis, but on the 
other hand a history of syphilis, ataxia, Argyll-Robertson pupil and 
severe sensory disturbances of a progressive character. Brain palsies 
are hemiplegic in distribution, spastic, painless, without muscular 
atrophy or involvement of the sphincters. Multiple sclerosis often 
resembles and sometimes even develops on top of a disseminated form 
of myelitis. The differentiation is extremely difficult when the spinal 
symptoms of multiple sclerosis are so prominent as to obscure the 
cerebral symptoms. In all cases the head symptoms should therefore 
be most earnestly sought for and if the case is one of multiple sclerosis 
there will be found some degree of optic atrophy, diplopia, dysarthria 
and tremor of the so-called intentional type. Cervical pachymeningitis 
is slow and progressive as a rule, but whether acute or chronic is char- 
acterized especially by the irritative and compression symptoms of a 
typical meningitis with the symptoms of the peripheral myelitis coming 
on later. 

Spinal meningitis is to be differentiated by the irritative root symp- 
toms, the tenderness of the spine upon pressure and the somewhat more 
marked febrile symptoms. The intense shooting pains along the course 
of the spinal nerves are characteristic. Moreover the paralysis and 
atrophy are not so segmental as neuritic in distribution. 

Hysterical paraplegia may have slight sensory symptoms, some 
atrophy and a spurious ankle clonus. The special stigmata of hysteria, 
the psychoneurotic character of the symptoms can scarcely be mistaken 
if care in the examination is exercised. 

Other forms of paraplegia are the senile from arteriosclerosis ; 
traumatic, from operations on the bladder, etc., and neuritic. 

Prognosis. — The outlook of every case of myelitis is problemati- 
cal. Unfavorable as it is in many of the cases, I am convinced that 
generally too pessimistic a view is taken in regard to its cure. Some 
cases, small in number to be sure, do get well, or at least recede and pass 
into a mildly chronic or latent condition. Some of these cases improve, 
then relapse or remit, then improve again only to relapse once more 
and so on until in the end they die in the usual way. The most hopeful 
cases are those that follow the acute infectious diseases, especially when 
the myelitis is of the disseminated type. Intermittent and malarial 
cases often recover. Syphilitic cases sometimes do. Gonorrhceal cases 
always get well under proper management. Tbe subacute, chronic, in- 
sidious, slow-progressing complete types are perhaps the most unfavor- 
able. Patients sometimes live many years with this type of disease. 



THE NON-NEUROXIC DISEASES 539 

The rapid cases, as a rule, soon cease to progress and even when asso- 
ciated with meningeal and neuritic symptoms are not unfavorable. 

Much depends upon the constitution of the patient, the amenability 
to cure of the underlying etiological disease like caries, tumor, etc., and 
the willingness to take treatment and the patience on the part of the 
individual afflicted. I have seen simple myelitis hurried to a fatal issue 
by injudicious electrical and "osteopathic" treatment. 

Dorsal myelitis is the most hopeful form of the disease from the 
■standpoint of the location of the lesion. Bedsores, cystitis and long- 
continued, complete paralysis are bad signs. Recession or disappear- 
ance of sensory symptoms is a particularly favorable sign and usually 
prophesies complete recovery. Death, when it comes on, usually is 
the result of exhaustion, cystitis and bedsores. 

Treatment. — The treatment of a case of myelitis calls for a high 
degree of patience and skill. The value of a masterly inactivity is 
sometimes most beautifully exhibited in the management of this trouble. 
On the other hand when there is a clear realization of the origin, nature 
and extent of the disease process a persistent, energetic treatment of 
the right sort will sometimes almost do wonders. Therefore unless 
the practitioner knows exactly what he is attempting to do, and is 
familiar with the best means of doing it, he had much better leave 
the case alone and do nothing. In this way he will at least escape 
the charge of having brought on a complete paraplegia and of having 
hastened the end. 

Under the best conditions the treatment of myelitis is not a grate- 
ful task; for it is slow and tedious and is punctuated by most surprising 
and at times thoroughly discouraging relapses. The patient had better 
be well forewarned of this before the treatment is undertaken and also 
be frankly told that he may have to lie in bed many months. 

The prime element in the treatment is rest, absolute rest, mental 
and physical. If we could but write a prescription for rest as we do 
for a drug, so as to bring it home to the patient's realization that in 
this disease rest, rest, rest, is of even greater therapeutic value than am 
drug, what better results might we not obtain! But t<> tell a patient 
to keep quiet and to do little but lie down for months and months 
seems so trite and inert that it is hardly to be wondered at that he 
rebels and demands some positive form of activity. Here is where a 
large part of the failure to successfully cope with myelitis is to he 
charged. I have had under my own care eases that under the a': 
to remain quiet were after several months progressing most satisfac 
torily. Trie symptoms were receding and the outlook was becoming 
decidedly hopeful. Too hopeful, unfortunately, for the patient fondl) 
imagining that he was about well, got up, started on a long W alk or 
some other prohibited exercise, only t<» hasten back to bed again in a 
few hours with the return of pains, numbness and muscular weakn 
I have had such experiences several times in the course en a 

single case. Under such circumstances the discouragement is 
that one is almost tempted to abandon the case and leave the patient 
to his fate. ( )n the other hand 1 have seen mosl happy results in c 
that were submissive and that maintained tin- prone p >siti *i for a 



54Q 



THE NON-NEURONIC DISEASES 



pericKi of time. Given such a willing patient, I do not relinquish all 
hope of cure, or at least amelioration, until some eighteen months have 
rolled around without any evidence of improvement. Cures have taken 
place even after such a long and discouraging experience as that. 

The second fact to bear always in mind in the early treatment of 
myelitis is that the disease process is an infectious inflammation. 
Elimination, therefore, is more important than counter-irritation. A 
diaphoretic treatment is preeminently called for in this progressing 
period of the disease. The bowels should be kept well open with calo- 
mel, salines and other forms of catharsis. The kidneys ma}- be stimu- 
lated by diuretin or other mild diuretic. The activity of the skin can 
be provoked by tepid spongings. Full baths had better be avoided 
until the disease has ceased to progress, and, even then they must be 
used cautiously and not too frequently. Only lukewarm baths are 
advisable, and generally they had better be half-baths given in bed and 
followed by gentle frictions. Hot and cold baths, or other form of 
hot and cold applications, are positively contra-indicated. Sea-bathing 
must be prohibited and treatment at the various hot springs and sana- 
taria is of very doubtful utility. They necessitate too much movement 
and are apt to be too stimulating. 

Counter-irritation of the spine is, in my opinion, of little benefit 
unless it is so mild that it can be used for a long period almost con- 
tinuously. Iodine, fly-blisters, vesicants of various sorts, the actual 
cautery and the seton have not been sufficiently beneficial in my obser- 
vation to encourage me in the use of them. Moreover, they have ad- 
ded too greatly to the general distress of the patient. I depend more 
upon the constant application of sinapisms, diluting the mustard some- 
times with ground flaxseed and changing them about on the back so> 
that the patient can wear them almost continuously. In this way they 
soothe the patient and relieve the pain ; above all they do not materially 
add to his discomfort. 

Among the remedies that may be employed, iodide of potassium 
still holds the first place. It must be used steadily and in moderate 
doses. In syphilitic cases the iodide in large doses and mercury are 
of course indicated. In the non-syphilitic cases of myelitis I am just as- 
urgent to contra-indicate the use of mercury as I am to indicate it in 
the cases of meningitis. If there are symptoms of meningomyelitis I 
use mercury steadily for a long period of time, guarding it with a small 
amount of opium. 

The use of opium or its alkaloid is sometimes advisable to relieve 
the pain and induce quietude for a time in the early management of 
the case. I have had no experience with ergot and cannot understand 
upon what principle it is recommended. Silver in the form of the 
nitrate has seemed to help some cases; so have the arsenite of sodium,. 
the salicylates, chloride of gold, and phosphorus. Later on small 
doses of strychnia, or the hypodermic injection of strychnia, may be 
employed to combat the paralysis. Cystitis must be carefully guarded 
against by clean catheterization and flushings and the use of buchu, 
boric acid, sandalwood and similar drugs. The skin around the scrotal 
region must lie carefully protected by a urinal or an antiseptic pad. 



THE NON-NEURONIC DISEASES 54I 

For bedsores as well as for the atrophic changes aggravated by am- 
moniacal urine, Palmer recommends the use of a soft linen bag large 
enough to extend down the thighs and filled with bran moistened with 
-dilute sulphuric acid. Two ounces of the dilute acid may be used 
to a quart of bran and it should be renewed every second day. 

Care in avoiding points of pressure, and the use of a water mat- 
tress or water pillows, will obviate the development of bedsores. 

Contractures cannot be forestalled, even morphine and hyoscin 
usually failing. A permanent bath is sometimes good for .them 
Tenotomy is of course to be considered in connection with severe forms 
of contracture. 

Special forms of myelitis sometimes call for special lines of 
treatment and such etiological factors as syphilis, malaria, etc., indicate 
the proper mode of medication. In chronic meningomyelitis much 
benefit is sometimes obtained from suspension and the spinal jacket. 
Stefano Personali especially claims good results from this treatment 
in this form of the disease. He employs the usual apparatus for sus- 
pension daily for one to four minutes for four days, then for four 
minutes for twelve days, after which the jacket is applied and worn 
in bed for three months. W 'hen the patient can walk a little about the 
house, this jacket is removed and another one applied. This is worn 
for two months, the patient not being kept so strictly in bed as before. 
A third jacket is then put on for three months, being made of strong 
muslin. In some cases the suspension may be made on an inclined plane 
and then the jacket be applied. 

Surgery may have a field of usefulness in myelitis aside from the 
mere removal of tumors, carious bone, etc. ; for in such operations the 
associated myelitis has been cured. 

In a case of typhoid myelitis in a young man, rest in bed with 
carefully arranged coordinating and resisting exercises, the exercises 
being continued and elaborated after he began to get out of bed, pro- 
duced happy results in a case of J. K. Mitchell. 

After recovery all cases must be urged to avoid that which may 
tend to bring on a relapse. Mountain climbing is therefore dangerous. 
A sea-voyage is excellent. A quiet, wholesome life, without strain 
and with plenty of fresh air and nourishing food must be sought after. 
In this way a recovered case of myelitis may live a normal age without 
airy- reappearance of the old symptoms. 

ACUTE ANTERIOR POLIOMYELITIS OF INFANTS. 

This is a common disease and is sometimes known as infantile 
palsy, acute atrophic spinal paralysis, or cornual myelitis. As it is 
primarily an inflammation it should he treated of under the general 
head of inflammations of the spinal cord. By some writers it is consid- 
ered among the systemic diseases of the cord, because the primary dis- 
ease process is limited to the column of gray matter that makes up the 
anterior horn, with mere secondary processes in the peripheral m 
neurones. In my own opinion, logical sequence demands that it should 
be distinctly ranked under the head of a localized inflammation of the 



542 



THE NON-XEURONIC DISEASES 









cord, for reasons which will appear when I discuss its pathology and 
pathogenesis. The disease is characterized especially by a flaccid 
paralysis and atrophy with certain consequent manifestations, the 
paralysis and atrophy being limited to individual muscles or groups of 
muscles, because of the damage to ' their representative cells in the 
anterior horns. 

Etiology. — The most striking feature of the etiology of infantile 
palsy is the age at which it occurs. Though it may appear at any 
period of life it is preeminently a disease of early childhood. The 
great majority of the cases occur in the second and third years, when 
the child is beginning to walk and is undergoing the process of denti- 
tion. The disease is very rare before the fifth month and is not often 
seen after the fourth year. According to Sinkler it has been known 
to start before birth, giving rise to a congenital type of the disease. 
It is slightly more frequent in boys than in girls. Heredity shows its 
influence, probably neuropathically, in a very small percentage of cases. 
It has occurred in several members of the same family. 

The great majority of the cases take place in the hot months of 
the summer. It would seem chat certain, time-honored alleged causes, 
such as sudden chilling of the body, over- exertion, traumata, etc., would 
be more operative at this time when the child is more out of doors 
and at greater liberty than in the winter when he is restrained and 
closely protected. And yet it is now pretty generally agreed that these 
supposed causes are subsidiary or at least especially operative in only 
a limited number of cases. 

The cause of infantile palsy is without doubt some form of in- 
fection, This is shown by the course of the disease, the circumstances 
under which it usually occurs, its appearance with other forms of in- 
fectious nervous diseases like cerebrospinal meningitis and neuritis, 
and by the fact that it has been not infrequently observed to occur 
epidemically. Moreover, micro-organisms have been introduced ex- 
perimentally into the bodies of animals and alterations have occurred in 
the cord that simulated perfectly those of, the disease under considera- 
tion. In addition to all this, the disease has followed other forms of 
infection such as scarlet fever, measles, whooping cough, etc. 

Most remarkable and suggestive, however, are the epidemics of 
anterior poliomyelitis that have been reported. In the outbreak in 
Vermont in 1894, reported by Dana, some 160 cases appeared from 
June to September in the country along the Otto Creek. In the same 
year Putnam reported an irruption that occurred in and about Boston. 
Medin, of Stockholm, described an epidemic in which there were 44 
cases in the same town within one month. 

That the disease is endemic rather than epidemic is suggested by 
the fact that Oppenheim voices when in his own particular experience 
he says that most of his cases have seemed to come from Weissensee, 
near Berlin. The Gloucester, Mass., epidemic that occurred in the 
summer of 1900, and was reported by Painter, occurred within a radius 
of four miles and included some 38 cases. 

The influence of sudden changes of temperature as a contributive 
cause along with the infection is strikingly shown in Painter's report. 



THE XOX-XEUROXIC DISEASES 543 

The majority of the cases occurred in, or more frequently twenty-four 
or thirty-six hours after, periods of extreme heat ; and in some in- 
stances immediately after a sharp drop from an abnormally high tem- 
perature, or a bath in the ocean. The disease has even attacked domes- 
tic animals, such as fowls, dogs and horses. In the Vermont epidemic 
a typical case occurred in a man seventy years of age. 

Pathology axd Pathogexesis. — The essential lesion in this dis- 
ease is an inflammation of vascular origin in the anterior gray horns 
of the spinal cord, with subsequent degeneration and disappearance of 
the ganglion cells and their processes. The work of Marie and Gold- 
scheider, Redlich and Siemerling seems to intimate that the process 
is primarily a general inflammation of the cord and that while the 
entire cross-section is involved the maximum point of the trouble is 
located in the anterior horns. An infection is the origin of the inflam- 
mation, the infectious material (an infectious embolus possibly) reaches 
the anterior horns by way of the anterior spinal artery. The peculiarity 
of the blood supply and the relative abundance of the ganglion cells 
in the lumbar and cervical portions of the cord, explain satisfactorily 
the preference of the disease for these localities, both in its pathology 
and symptomatology. 

The macroscopic and microscopic appearance of the cord and lesion 
will vary according to the period of the disease in which the examina- 
tion is made. Most of the earlier examinations of Charcot and others 
were made in the later stages when the inflammation had long sub- 
sided and only the atrophic condition was in evidence, and explain 
the earlier teaching, now known to be erroneous, that the disease is 
primarily a parenchymatous inflammation of the ganglion cells of the 
anterior gray horns. Since the investigations made by (ioldscheider, 
Siemerling, Dauber, Marie, Redlich, Von Leyden, Schultze and others 
we now know that the disease process is primarily a vascular inflamma- 
tion with the atrophic changes occurring as secondary results. In the 
first stage, therefore, we find hyperemia, proliferation of the terminal 
branches of the anterior spinal artery, dilatation and hypertrophy of the 
vessels, perivascular effusion and exudation, thrombotic obstruction, 
extravasations of blood, and leucocytosis. There is a heaping up of 
the round cells about the vessels and a clouding of the elementary 
structures. Xo suppuration occurs. The outlines of the horn are ob- 
scured ; it looks swollen, and in many cases the adjacent parts of the 
cord and meninges are softened and congested. As the process ad- 
vances, the ganglion cells become hazy, swollen and involved in an 
incipient chromatolytic change. Their processes are swollen and exhibit 
a beginning degeneration. Later on the cells and fibres arc distinctly 
atrophied. Some of them disappear entirely and their places taken in 
part by an overgrowth of connective tissue. The involvement of the 
neighboring white substance decreases. The anterior horn diminishes 
and shrivels and the cord seems in the vicinity smaller and harder. 
Sometimes there is an associated sclerosis in the lateral columns. The 
anterior roots and motor nerves, of course, are atrophia 1 and the re- 
lated muscular tissues arc wasted and show an overgrowth of con- 
nective tissue. Alterations of this same character have been observed 



544 THE NON-NEURONIC DISEASES 

in the motor nuclei of the medulla oblongata, since these nuclei are 
but the upward extension of the anterior gray matter of the cord. 
When the disease is among the lower medullary nuclei it is known 
as inferior polioencephalitis ; when among the upper or nuclei of the 
motoroculi, it is spoken of as superior polioencephalitis (ophthalmo- 
plegia). 

It is to be noted that the branches of the anterior spinal artery 
are, in Cohnheim's sense, terminal arteries and that, as Schaefer has 
shown, no one set of arterioles is limited in its distribution to any one 
group of cells. The supply of the posterior parts of the cord by the 
posterior spinal arteries is comparatively scanty. These facts help to 
explain the peculiar limitation of the maximum focus of the disease 
to the anterior or motor part of the cord and the symptoms of paralysis 
and atrophy in particular muscles or groups of muscles. 

Symptoms. — The symptomatology of acute anterior poliomyelitis 
is marvelously definite and uniform. The clinical picture develops and 
progresses through stages that are singularly distinct and logical. A 
typical case, except in the very earliest onset of the disease, presents no 
great difficulties in diagnosis. Remembering the pathology, one can 
readily understand why every case should show progressively the fol- 
lowing four symptomatic stages, namely, (i) infectious fever, (2) 
widespread, sudden, flaccid paralysis, (3) recession of the widespread 
paralysis with permanent paralysis and atrophy in certain individual 
muscles, and (4) deformities resulting from wasting of the muscles 
and contractures. 

Such is the regular clinical picture and progress of infantile palsy. 

I will now discuss the symptoms of these four stages of the dis- 
ease a little more in detail. 

The beginning of the disease is usually abrupt and unexpected. 
After a happy day with its playmates, romping in the open air, the 
child comes in and complains of extreme weariness and distress. Its 
head begins to ache. It is nauseated and may vomit. It is listless and 
clings to its mother's arms. Perhaps it has a violent chill. The face 
becomes hot, dry and flushed. It may soon become stuporous and even 
slightly delirious. There may be a general convulsion. The child re- 
fuses all food and in every way shows that it is decidedly sick and 
feverish. With or without the advice of the family physician, the 
mother regards and treats the condition as probably a cold, an acute 
attack of indigestion, distress from the teeth or the possible beginning 
of an attack of measles. It is put to bed and passes a feverish and 
restless night. The temperature has been anywhere from 102 degrees 
to 104 degrees F. In the morning the child wakes with perhaps a 
slight diminution of the febrile symptoms but completely paralyzed in 
the legs or arms. This is the frequent way that the disease starts. 
The febrile stage lasts from a few hours to a few days. Sometimes 
it is so brief and the paralysis comes on so suddenly, that one involun- 
tarily thinks of a hemorrhage. At other times it is so prolonged that 
for many days no diagnosis is possible. For his own credit's sake, 
the physician will always, in such doubtful cases, keep in mind the 
possibility of acute poliomyelitis and inform the family of that pos- 



THE NON-NEURONIC DISEASES 543 

sibility. To the average layman paralysis is a most awful disaster, and 
though, when the paralysis comes on, the physician may assure the 
family that it will in a large measure disappear or recede, it will not 

FIGURE 116. 




Anterior poliomyelitis, showing atropine condition of the righl leg. \)v. 
Fitch's ease. 

restore' the confidence shaken by the shock of seeing their child sud- 
denly paralyzed and by their not having been forewarned of such a 
possibility. 

When the paralysis is discovered the general febrile disturbance 



546 



THE NON-NEURONIC DISEASES 



has usually subsided somewhat. There may be some rheumatoid pains 
complained of in the back and extremities for a few days, or there 

FIGURE 117. 




Anterior poliomyelitis, showing the atrophic condition of the right Kg. 

may be retention of urine or some slight gastrointestinal trouble. The 
paralysis, however, is the dominant symptom. This is flaccid and 



THE XOX-XEURONIC DISEASES 547 

complete from the beginning. Usually it is paraplegic in distribution, 
involving both legs entirely. Sometimes it involves only one leg, or 
one leg and one arm, or one arm alone, or both arms. Paralysis of one 
leg or of one arm is by far the most frequent way it appears. Paralysis 
of both legs is perhaps the third most common distribution. Paralysis 
of the four limbs, quadriplegia, or of the two arms alone, crossed 
paralysis, or hemiplegic paralysis, is very rare. Usually the paralysis 
includes the whole limb and reaches its height in a few hours or a few 
days. In a short time it is noticed that some of the muscles of the 
limb are regaining their mobility while others continue immoble. In 
other words the volition of the patient can exercise itself upon some of 
the muscles or muscle-groups but not on others. The extreme paralysis 
in the latter may last from six to eight weeks, when there is a little 
recession in their paralytic state. These muscles now begin to degene- 
rate, waste and undergo a progressive and rather rapid atrophy. Their 
electrical examination reveals the phenomena of the reaction of de- 
generation. The reflexes in which the atrophied muscles are concerned 
are lost. 

These four symptoms, flaccid motor paralysis, loss of the tendon 
reflex, atrophy and the reaction of degeneration are pathognomonic of 
disease of the lower or peripheral motor neurones. Hence the pre- 
eminent characteristic of the paralysis of infantile palsy is that it is 
a degenerative one, and that it picks out particular muscles and muscle 
groups. The muscles of the leg that are mostly affected are those of 
the anterior tibial group. Sometimes only the extensors of the leg are 
involved. The sartorius usually escapes. In the arm the deltoid and 
shoulder muscles are chiefly inplicated. The deltoid may be paralyzed 
alone, or in combination with the biceps, internal brachial and supinator 
longus. All kinds of combinations are possible. In a few cases the 
motor cranial nerves have been included. A slow improvement, may 
take place in some of these muscles up to the end of a year. After 
that no further improvement is to be expected. Gowers says that we 
should never forget that after six months the lesion in the cord has 
practically become a cicatrix. 

There are no sensory symptoms that belong to this disease. Some- 
times in the beginning there are dull pains of a rheumatoid character 
in the muscles. If these pains become severe or the muscles arc 
unusually tender on pressure, there is probably some degree of peri- 
pheral neuritis with the poliomyelitis. In a word the sensations are 
absolutely normal in uncomplicated infantile palsy. The slight de- 
crease in sensibility in the paralyzed limb is undoubtedly due to the 
vasomotor disturbance and lowered temperature of the skin. Some- 
times this decrease of surface temperature amounts to several degrees 
and is associated with a bluish, mottled appearance of the skin. 

There are no psychic troubles excepl the earl) febrile stupor and 
delirium and the sphincters arc never involved. 

The whole limb ceases to grow as rapidly as the well limb; the 
bones do not continue to develop: and as a result the whole extremity 
appears stunted, shortened and awkward in movement. ( )n account 
of the atrophy and contractures in certain of the muscles, antagonistic 



548 



TIIK N ON -NEURONIC DISEASES 



groups do not work together as they should and deformities and curva- 
tures result. Talipes equinus, talipes varus and valgus are thus pro- 
duced, as well as deformities about the knees and curvatures in the 
spine. The most common form of foot deformity is pes equino-varus 
on account of the paralysis of the extensors of the foot and toes. When 

FIGURE 118. 




Anterior poliomyelitis, showing the wasting of the right leg and foot-drop. 

the tibialis anticus alone is affected, there is a condition of talipes valgus. 
When the calf muscles are stricken, pes calcaneus obtains. The claw- 
hand is a far less frequent form of distortion than are any of those 
of the feet. In the spinal column there may occur lordosis or scoliosis. 
Diagnosis. — In the early or febrile stage the diagnosis of acute 
anterior poliomyelitis is always uncertain and sometimes quite impos- 



THE NON-NEURONIC DISEASES 549 

sible. Even after the discovery of the paralysis, there may be doubt 
as to the exact cause of it. Very rarely, therefore, is the diagnosis 
of infantile palsy ever made early. The symptoms at this period of 
the disease are made light of. They are attributed to dentition, gastro- 
intestinal trouble, over-exertion and heat, intestinal parasites or some 
other trifling ailment. The parents are assured that the little one will 
soon be all right. One can easily imagine the feelings of the parents 
and the chagrin of the physician under these circumstances when the 
paralysis is recognized at last. 

The early diagnosis of the disease is most desirable therefore for 
more reasons than one. The physician will do well to remember that 
the paralysis is the special, significant symptom and after forewarning 
the family, be on the alert for the first indication of it. It usually comes 
on quickly, even sometimes with the beginning of the fever, rarely 
later than a few hours or days. An appearance of weakness, listless- 
ness, exhaustion, disinclination to move the limb should be prompt to 
awaken suspicion. A close examination will sometimes show very 
early a little more voluntary mobility on one side than on the other. 
Such indications, faint as they may be, had better be regarded as the 
forerunner of a paralysis than be erroneously attributed to the mere 
malaise of the febrile state. 

When the paralysis does frankly declare itself, certain characteris- 
tics about it render the diagnosis certain. Its suddcimess of onset, its 
completeness from the beginning, its involvement of one of the limbs 
with later limitation to particular muscles, its gradual improvement, 
and its association with atrophy, loss of reflex action and the reaction 
of degeneration render its nature perfectly clear. 

In the later stages of the disease, the history of the case, the local- 
ization of the paralysis, the muscular atrophy, the vasomotor disturb- 
ances, the retardation of growth and the contractures and deformities 
in the limb make the diagnosis positively easy. 

A few atypical forms of the di sense may cause some confusion in 
differentiating them from hematomyelia, acute rachitis, coxitis, osteo- 
myelitis, syphilitic pseudo-paralysis, acute myelitis, acute disseminated 
myeloencephalitis, birth palsies, cerebral pals; \e muscular 

atrophy, lumbar spinal gliosis, congenital muscular defects, and multiple 
neuritis or neuritis of special ner- 

In hemorrhage and acute myelitis there are prominent sens 
symptoms, exaggerated reflexes, involvement of tin- sphincters and 
bedsores. Hemorrhage, of course, is sudden but does not occur often 
without trauma. Moreover the paralysis is not preceded by or im- 
mediately associated with a fever. Myelitis is slower in its onset; its 
fever is not so high usually and is longer in duration ; its paralysis d<>es 
not recede and remain permanent in particular muscles as it 
poliomyelitis. It should be remembered in this connection, however, 
that the earliest symptoms of infantile palsy are so indicative of a trans- 
verse myelitis in many cases that some authorities believe that tl 
of anterior poliomyelitis begins as a mor< complete transv 

myelitis of a mild degree, with the infiammati receding, except 

from the anterior horns where its maximum foci were located. I his 



55° THE NON-NEURONIC DISEASES 

is doubtless the explanation in part of the early sensory symptoms like 
the rheumatoid pains often complained of in poliomyelitis and of the 
initial paraplegic-like distribution of the paralysis. The hyperaesthetic 
condition of the involved limb during the first few days of the disease 
is of much assistance in the making of the diagnosis. Of course as the 
inflammation subsides these sensory manifestations disappear and as 
I have said above the further course of the disease is notable for the 
complete absence of sensory phenomena. 

As Oppenheim has well pointed out acute rachitis, coxitis, and 
osteomyelitis are distinguished from the early stage of poliomyelitis by 
the resistance offered by the child when passive movement is attempted. 
He contracts his muscles and holds them in a state of rigidity to avoid 
the pain of movement. 

Syphilitic pseudo-paralysis is to be established by the history of 
infection, other signs of specific disease, and the character and distribu- 
tion of the paralysis. 

Cerebral palsy comes on abruptly, is hemiplegic in character and 
is accompanied by rigidity and exaggeration of the reflexes. There is 
mental depression of a profound sort and stupor, while a series of local 
or Jackson i an convulsions may occur. 

Birth palsies are flaccid and degenerative and involve usually only 
the arm. 

Progressive muscular atrophy rarely occurs in children. It is 
gradual in its onset, slow and steady in its progress, without febrile 
or sensory phenomena. 

Peripheral neuritis, and especially multiple neuritis, are rare though 
they do occur in children alone or as complications of poliomyelitis. 
The similarity of- many of the symptoms sometimes leads to much 
difficulty in the making of a differential diagnosis. They are more 
gradual in onset than infantile palsy, are marked by local pain and 
tenderness on pressure and have slight or no febrile phenomena. When 
there is fever it lasts longer than the fever of poliomyelitis. The 
paralysis assumes the bilateral type in multiple neuritis and the mono- 
plegic type in simple neuritis. It is tardy in its development as com- 
pared with the paralysis of poliomyelitis. The atrophy is not quite 
as pronounced and is slower in appearing, while vasomotor disturbance 
such as oedema may be present. In neuritis there is a greater tendency 
of involvement of the cranial nerves. It is to be remembered that 
peripheral neuritis and poliomyelitis may be associated in the same 
patient. 

Prognosis. — The prognosis of acute anterior poliomyelitis in re- 
gard to life is absolutely favorable. In regard to the recession of the 
paralysis in part and improvement within the first six months or a 
year it is favorable. In regard to any further improvement after the 
first year it is absolutely bad. 

Death has been reported in the first stage, possibly by involve- 
ment of the bulbar nuclei or other complication. Neither the disease 
nor its sequelae cause a fatal issue except in the rarest instances. A 
few complete recoveries have been observed. Improvement — and some- 
times a great deal of improvement — is what may be usually looked for. 



THE NON-NEURONIC DISEASES 55 £ 

The amount and character of the improvement, and the degree and 
nature of the sequelae, can be influenced by the early treatment. Elec- 
trical examination helps much in forecasting the probable improvement. 
Muscles that still respond to the faradic current after two or three 
weeks will resume their normal functions. When they show the re- 
action of degeneration they will remain paralyzed and later on become 
atrophied. 

Treatment. — The early treatment of infantile palsy is antipyretic 
and constitutional; the middle treatment \sneurological and orthopaedic ; 
the later treatment is orthopedic and surgical. 

In the beginning of the disease the clinical picture is that of an 
infectious fever. Every effort at this time should be made to check 
the infective inflammation. The child should be put to bed and kept 
absolutely at rest. The bowels should be opened freely with calomel ; 
the kidneys stimulated by some simple diuretic ; and the skin kept active 
by the use of hot drinks and warm coverings. A few leeches may be 
used on the spine, or mustard or iodine applied. It is useless and in- 
advisable in an infectious inflammation of this sort to apply extreme 
heat or cold to the spine, as is done is meningitis. The spinal ice bag 
should never be used. Full baths, hot or cold, produce too much dis- 
turbance and excitement ; do very little good ; and may do a great deal 
of harm. The fever can best be controlled by aconite and sweet spirits 
of nitre. The salicylates and belladonna in full dosage have been recom- 
mended in this initial stage of the disease. I have found rest and 
quiet, gentle but steady elimination, with mild local counter-irritation 
with mustard the most advantageous way of managing the first or 
febrile stage. 

Usually the paralysis is complete, and has existed for some little 
time when the patient first comes under medical observation. The treat- 
ment now becomes almost entirely mechanical. It consists of the steady 
use of massage, aided by electricity. Of course the patient's general 
health and nutrition must be kept up, but except for assisting in doing 
this the further use of drugs is uncalled for. As the result of my 
own personal observation, I consider the steady use of massage the 
prime factor in the management of this stage of the disease. Every 
day, sometimes twice a day, I have the paralyzed limb rubbed and 
stroked up towards the body. The hand of the operator may be well 
oiled with olive or cocoanut oil. Ten minutes should be occupied in 
each seance. The muscles later on may be kneaded as well as stroked. 
Passive movements of the limb should be instituted early and gymnastic 
exercises with slight resistance to the movements should he persistently 
carried out to avoid as much as possible the late contractures and de- 
formities. It may even he necessary to use stiff bandages, splints, rub- 
ber muscles and other forms of apparatus t<> assist in this. The early 
and persistent treatment of these cases in this way cannot be too stren- 
uously insisted upon. Many of the later deformities and 1<<ss ,»i' function 
are due to the neglect or had management of these eases in the begin- 
ning. Massage and electricity may be cautiously begun as early as two 
weeks after the first appearance of the paralysis. 

'Hie use of electricitv two or three times a week at first, and then 



55 2 THE NON-NEURONIC DISEASES 

daily, is highly commendable. The only rule is to employ that cur- 
rent and that strength that will just produce a muscular contraction. 
If the galvanic current is used the cathode may be placed anywhere 
upon the body, while the anode is applied to the affected muscles. Use 
mild currents at first and increase gradually to the point of causing 
muscular contraction. The child must not be allowed to get frightened. 
When contraction can be obtained with the faradic current, it is to be 
preferred. Static electricity is useless. The electricity need not be 
applied longer than for two or three minutes at each sitting and after 
every two or three weeks' treatment, it is well to allow a week or two 
of rest without the electricity. 

In this way the massage and electrical treatment should be kept 
up for a year and at occasional intervals during the next year. After 
that it is of no further use. 

I regularly advise the frequent immersion of the limb in warm 
water, say from 90 degrees to 95 degrees F. I have had no experience 
with the subcutaneous injection of strychnine, as has been sometimes 
recommended. 

If the' above line of treatment be started early and carried out 
with care and watchfulness there will be comparatively little in the 
way of deformity. Many cases are so neglected, however, that the 
deformities become so prominent that orthopaedic and surgical measures 
have to be invoked for their relief. Tenotomy and the wearing of 
plaster casts and specially fitted apparatus are the measures employed. 
The methods of doing this are described in the books upon surgery 
and orthopaedics. When a shortened tendon has been cut and an 
extension apparatus fitted to the limb, it must be carefully noted that 
the latter is comfortable, does not impede the circulation, cause pres- 
sure or chafe the skin. It must be changed as the limb grows. Some- 
times the plan of Drobnik may be tried of partial or complete trans- 
plantation of the tendon of a paralyzed muscle to a neighboring healthy 
muscle. 

POLIOMYELITIS OF ADULTS. 

The only excuse for devoting a special section to the considera- 
tion of anterior poliomyelitis in adults is that it is so comparatively 
rare and that its clinical exhibition varies slightly from that of the more 
common infantile form of the disease. It occurs in adults as an acute, 
subacute and chronic affection. 

Etiology. — The' disease occurs more frequently in men than 
women and between the ages of twenty-five and thirty-five. It is be- 
coming more and more conclusively established that the predominant 
cause of the disease, in practically all cases, is an underlying toxaemia. 
The acute infectious fevers, especially measles, the puerperium, severe 
gonorrhoea, etc., have been followed by acute poliomyelitis. An under- 
lying toxic state of the blood has probably co-operated with exposure 
to cold, over-exertion, and traumata, to which the disease in some 
instances has been attributed. The subacute and chronic cases have 
been associated with exposure, syphilis, lead-poisoning and diabetes. 
Oppenheim once saw an acute case follow prolonged chloroform nar- 



THE NON-NEURONIC DISEASES 553 

cosis. As these same causes play a large role in the production of 
multiple neuritis, and as this form of poliomyelitis has been less fre- 
quently noted since we have learned that polyneuritis is responsible for 
many of the symptoms, caution must be exercised in the diagnosis espe- 
cially when a frank intoxication is existent. 

Pathology and Pathogenesis. — In the few cases that have been 
examined after death the pathological findings were identical with 
those seen in the infantile form of the disease. The gray matter of 
the anterior horns revealed a condition of primary acute or chronic 
inflammation, with secondary degeneration and atrophy of the nervous 
elements. In some quarters the belief is growing that a primary wast- 
ing of the cells is provoked in some of the severer toxsemic cases and 
that the inflammation and vascular changes are secondary, or rather 
concomitant, phenomena. At all events the two associated processes, 
vascular inflammation and cellular atrophy, constitute the pathological 
basis. The white matter remains unaffected or is only slightly degen- 
erated secondarily. 

Symptoms. — The onset of the acute cases is the same as that in 
the infantile forms of the disease except that the early fever lasts a 
little longer, one or two weeks, some pain especially in the back is more 
apt to be present, and the initial paralysis is more widely extended. 
If there is pain in the limbs a polyneuritis is probably present. The 
beginning of the subacute and chronic cases is insidious, usually with- 
out febrile phenomena and pain and without the usual initial tem- 
porary extensive paresis. 

In the acute cases the paralysis appears about the time that the 
fever is subsiding. At first it is widely distributed, though not equally 
profound everywhere. Gradually this recedes leaving some groups of 
muscles completely paralyzed while others regain their normal power 
of action. The paralysis is flaccid and is remarkable for picking out 
individual muscles or groups of muscles. Sometimes a whole limb may 
be involved and more frequently it is the leg. In a few days the re- 
action of degeneration can be elicited by an electrical examination of 
the diseased muscles. They begin to atrophy and feci soft. ( )n account 
of fatty degeneration they may assume the appearance of a pseudo- 
hypertrophy. The paralysis may partially recede even in them during 
the course of the first month or so. They never, however, undergo 
complete recovery. If they do recover the trouble was probably due to 
]>eripheral neuritis. The further progress of the disease is the same 
as it is in acute anterior poliomyelitis of children. 

In the chronic type of the disease there is merely an initial weak- 
ness in the legs or tlu* arms, which progresses slowly and gradually 
towards paralysis. Usually one <>r two limbs, and more particularly 
certain groups of muscles in them, only are paralyzed. In other ca 
all four extremities may be involved. The paralysis is flaccid, dec! 
atrophic and associated with electrical reaction of degeneration and loss 
of reflex action if the muscles concerned in the reflex arc arc implicated. 
Almost any muscle or muscle group in the arm or leg ma} be aftli 
and it is therefore needless to specify. Fibrillary twitching is often 



554 THE XOX -NEURONIC DISEASES 

present and annoying. There are no other symptoms in typical cases 
though sometimes dull aching pains are complained of. 

The disease is so varied in its manifestations that an effort has 
been made to establish particular types. This it seems to me is un- 
necessary though it is well to remember perhaps that some cases ad- 
vance rapidly to a climax, then recede and ultimately return to almost 
complete health. Other cases advance slowly and with sharply limited 
atrophy and paralysis, causing them to bear a striking resemblance 
to progressive muscular atrophy. In still other cases there is a less 
rapid but more steady advance of the trouble until death occurs in a 
year or two. 

In. all of these forms of the disease there are resemblances of a 
striking sort to multiple neuritis, progressive muscular atrophy, acute 
ascending myelitis, Landry's paralysis, etc. Indeed it is beginning 
to be strongly suspected that some of these latter affections, either in 
part or whole, are poliomyelitic. 

Diagnosis. — The symptomatic diagnosis of poliomyelitis is readily 
made even though the case is not strictly typical ; the pathological diag- 
nosis, however, is often a matter of the greatest difficulty. The etiolo- 
gical precedents, the initial fever and paralysis, the distribution, char- 
acter and progress of the latter, the muscular atrophy, the electrical 
reactions and the absence of sensory symptoms are distinctive if studied 
en masse in the clinical presentation of the case. The underlying cause 
of these symptoms, however, may be confused with polyneuritis, pro- 
gressive muscular atrophy, amyotrophic lateral sclerosis and gliosis. 

In polyneuritis there are peripheral and local pains in the nerves 
and muscles of the limbs. There is ataxia. The paralysis is not so 
sharply elective but involves the ends of the lower limbs first, gradually 
ascends and ultimately attacks the arms in the same way. Other nerves 
besides those of the extremities, as for example the cranial nerves, may 
be involved in neuritis. There are some cases, however, in which a 
differential diagnosis is quite impossible. This is probably due to the 
fact that in toxic cases there may be both neuritic and poliomyelitic 
processes going on at the same time. Not a few authorities believe that 
in some of these cases, if not all of them, the peripheral, neuritic de- 
generative process is a mere secondary result of a profound toxic dis- 
turbance in the anterior cornual cells and their nutritive function. 

Progressive muscular atrophy is especially liable to be confused 
with chronic poliomyelitis. It is to be remembered, however, that a 
low grade poliomyelitic process possibly underlies many of the spinal 
atrophies. In typical progressive muscular atrophy the atrophy runs 
ahead of the paralysis and not vice versa, as in poliomyelitis. Moreover 
there is no real initial stage as in the latter disease and the atrophy 
usually begins in the small muscles of the hands. 

Amyotrophic lateral sclerosis is characterized by increased reflexes, 
a less degree of atrophy, selection of the arms with merely early weak- 
ness in the legs and marked bulbar symptoms. In general gliosis 
sensory symptoms are prominent and there are trophic manifestations 
in the skin as well as the muscles. 

Prognosis. — The prognosis is good in pure cases so far as life is 



THE NON-NEURONIC DISEASES 555 

concerned. In regard to the paralysis, the hope of a considerable de- 
gree of restitution may be held out up to a month or two after the 
onset of acute symptoms. Some cases may even partially recover after 
that or until a year or two has rolled around. Complete recovery is 
so exceptional as to almost warrant the assertion that it is never to be 
expected. As the outlook for the paralysis in multiple neuritis is 
peculiarly favorable, the more nearly these cases of poliomyelitis ap- 
proach a multiple neuritis the more hopeful is their prognosis. Death 
is not a common result of this disease. 

Treatment. — The management of these cases is practically the 
same as it is in the infantile form. 

ABSCESS OF THE CORD. 

Abscesses rarely form in the spinal cord as they do in the brain. 
Only a very few cases have been put upon record, and they followed 
purulent spinal meningitis of both the cord and brain, or were the re- 
sult of a metastatic transference of the disease from some near or 
remote focus of suppuration. Myelitis scarcely ever goes on to the 
production of an abscess. Putrid bronchitis, gonorrhoea, abscess of 
the prostate gland and traumatism have seemed to be responsible for 
it in some cases. Minute collections of pus have been noted in a few- 
instances of poliomyelitis. The gray matter is usually the seat of the 
abscess, especially when associated with purulent meningitis. In such 
cases the brain is very often also the seat of the suppurative process. 
The majority of the abscesses appear in the upper part of the cord 
though they may locate anywhere. 

Paraplegia, anesthesia, sphincter paralysis, girdle pains and all 
the usual signs of a severe meningoniyeiilis are present. Weakness, 
tremor and incoordination in the arms have been seen in other case- 
along with the symptoms in the lower extremities. The usual signs 
of infection are commonly present, such as the irregular fever, the 
chills, the foul tongue, the subnormal temperature, the debility and 
general typhoid state. 

The diagnosis is easy as a rule but the localization of the .ib- 
is extremely difficult. 

As the condition is associated usually with a diffuse, or general 
septicaemia, surgical intervention would be of little avail. Death usu 
ally takes place- in a few da; 

TUMORS I IF Till-: SPINAL C< >RD. 

By the term tiunor i do not mean all forms of excrescences and 
protuberances that may compress the o>nl <>r damage it anatomically 
and functionally within a limited ana. Tin symptoms of these may 
at times be identical with those of tumor. The ultimate results upon 
die cord may even Ik- tin- same. Vertebral disease, displacements, 
caries and exostoses of syphilitic or traumatic origin may affect the 
cord and its membranes very much as a tumor would. Focal hem 
orrhage. thrombosis, embolism, may in their after effects exhibil an 



55& THE NON-tfEURONIC DISEASES 

obscure resemblance to a spinal neoplasm. This is because at times 
all of these troubles may be limited and unique, though obscure in 
their symptomatology, while obscurity and total absence of symptoms 
obtain sometimes even in tumor. These conditions must therefore 
always be carefully excluded in the diagnosis. 

By tumor of the spinal cord I mean those circumscribed morbid 
growths that appear in the spinal canal and spring from the membranes 
or develop within the cord substance itself. The interest in these for 
a long time was merely pathological and post mortem. Erb suggested, 
in 1878, that they might be operated upon. It was the successful case 
of Gowers and Horsley, in 1887, however, that renewed the interest 
in these conditions and caused them to be studied clinically so thor- 
oughly that now a fairly definite symptomatology attaches to them. 
They certainly offer a more tempting field for the surgeon than do the 
brain tumors. Disheartening as are the total results of operative pro- 
cedures, and especially of medical treatment in both, the results are 
better in the tumors of the cord than they are in those of the brain. 
This is significant in view of the fact that the literature would seem 
to indicate that the latter are much more common than the former. 

Etiology. — This is not the place to go extensively into the etiol- 
ogy of tumors. Outside of certain diathetic conditions, like syphilis 
and tuberculosis, congenital influences as observed in certain glioma- 
tous and fatty tumors, parasites like echinococci, and a few obscure 
traumatic incidents, we know very little about their causation. Wet 
and cold have been followed by the sudden appearance of their symp- 
toms but it is probable that these agencies merely provoked the men- 
ingitic, myelitic and other secondary accompaniments of them. Mul- 
tiple tumors exhibit a faint degree of heredity. Most all spinal tu- 
mors appear between the ages of thirty and fifty. Tuberculous tu- 
mors appear earlier. Men give a history of them more often than 
women. The etiological incidence that belongs to the tumor per se is 
not materially altered by its being located in the spinal canal. 

Pathology and Pathogenesis. — A tumor may arise from the 
vertebrae, the spinal membranes, or the cord itself. All kinds of neo- 
plasms occur, though there are differences in regard to the frequency 
of certain types and their location. The great majority of them are 
meningeal in origin ; next in frequency arc the intraspinal ; 
least in frequency are the vertebral. Glioma and sarco)na 
are the commonest, and next after them fibroma, myxoma, 
gumma and tubercle. Some of the tumors manifest a choice of loca- 
tion and it is always well to try and differentiate those that are be- 
tween the bony column and dura (extra-dural), those between the 
dura and cord (intra-dural), and those that are within the cord itself 
(intra-medullary). There is a slight difference in their symptoma- 
tologies. 

Extra-dural growths may originate in the membrane, the tissue 
between the membrane and bone, or outside and grow in through the 
inter-vertebral foramina. The parasitic tumors, echinococcus and cys- 
ticercus, occur here. Lipomata usually select this site. 

The intra-dural tumors are sarcoma, myxoma, psammoma, fibro- 



THE XOX-XEUROXIC DISEASES 



55! 



ma. syphiloma and tubercle. A sarcoma may be single and extended 
or multiple. Rarely tubercular and parasitic tumors have been seen 
within the meshes of the arachnoid. Myolipomata have been found 
here also. Multiple neuromata sometimes occur on the nerve roots. 

The more, common intra-medullary growths are the gliomata, syph- 
ilomata. sarcomata and tubercle. Every variety of neoplasm has de- 
veloped within the cord. These tumors are single or multiple and 
spring from the pia mater or the wall of the central canal. 



FIGURE 119. 




FIGURE 1 jo. 




Tumor of the medulla spinalis. 
• r Braubach. ) 



Tumor in the dura of the upper 
part <>f the lumbar enlargement. 
( After < iowers 



The size- of these growths i> necessarily small, ranging from that 
of a pea to an inch or two in length and an inch in thickness. Some 
spread longitudinally along the cord, notably the gliomata, which ma) 
tch the entire spinal length. The sarcomata also diffuse them 
selves btu not quite so much as the gliomata. Sometimes the tumor 
ensheaths tin- cord as in a tube. 

The iifpcr and lower dorsal regions of tin cord are the favorite 
location of tumor. The morbid growths that attack the Cauda i'<]ui>i<i 
are rather frequent and large relatively. In tin- neighborhood of the 
tumor the shape of the cord i- altered. I lie c^v\ will M it tlie 



558 



THE NON-NEURONIC DISEASES 



tumor is a soft one, but as a rule the tissues are denser and harder than 
normal. Extra-medullary tumors rarely absorb the substance of the 
cord, though they may press it extremely out of shape. Intra- 
medullary tumors both absorb and distort the spinal tissues. Some- 
times the intra-spinal tumors are sharply demarcated ; at other times 
they shade off into the normal tissue. The latter may be but little 
altered at times but usually it is the seat of secondary alterations, inflam- 
mation, softening, hemorrhage, etc. 

Symptoms. — There is a certain degree of constancy and uniform- 
ity about the symptomatology of all tumors, and as that is often as far 
as we can carry the diagnosis, the exceptional differentiations are only 
possible in a limited number of cases. 

For operative purposes a differential diagnosis between extra- 
and intra-dural tumors should always be attempted. The former pro- 

FIGURE 121. 










Neuroma of the cauda equina. (After Lanceraux.) 

duce more particularly pressure symptoms and are often accompanied 
by pronounced root symptoms, local tenderness of the spine and evi- 
dences of bone disease. The latter add to these, signs of greater im- 
plication of the cord itself, pressure, irritative and destructive. Intra- 
medullary tumors are not marked by such severe initial pains as are 
the meningeal tumors, and their motor phenomena are more prone to 
be unilateral, especially in the beginning. Nevertheless it must be 
admitted that in most cases only an approximation can be attained in 
these differential diagnoses. Fortunately such refinement of diagnosis 
is not absolutely called for in the majority of the cases. 

The two essential points to be established in the diagnosis are ( I ) 
the actual presence of a tumor, and (2) its longitudinal or segmental 
position in the cord. 

In the order of their usual development the symptoms of a spinal 
tumor are sensory, motor, visceral, trophic and topical. The first to 
appear are the signs of spinal root compression and irritation. This 
consists of constant, severe and continuous neuralgic pain shooting 
along the course of the spinal nerves. About the trunk there is uni- 
lateral or bilateral intercostal neuralgia. Sometimes there is a typical 
girdle sensation. Sharp, lancinating pains may shoot down the arm. 






THE NON-NEURONIC DISEASES 559 

more rarely in the legs. The nerve trunks themselves are not sensi- 
tive to pressure. These pains have caused such mistaken diagnoses to 
be made as appendicitis, gallstone colic, indigestion and angina pec- 
toris. In not more than ten per cent, of the cases are these charac- 
teristic pains absent. Their course is highly suggestive. For instance. 
slight at tirst, they become keen and penetrating, and paroxysmal, 
then finally continuously dull but with sharp exacerbations. They are 
listressing that they have driven their victims to suicide. They con- 
tinue throughout the entire course of the disease. Pain may be pres- 
ent in the spine if the tumor is one of the dura; not so if it is intra- 
medullary. 

Hyperesthesia very often accompanies the pain. Between the 
exacerbations various parcesthesicc may be present, such as numb: 
tingling, pins-and-needles sensation, formication. These posterior root 
is may occur just as prominently when the tumor is in the anterior 
part of the cord as when in the posterior part and actually in touch 
with the posterior roots. Later on anccsthesia takes the place of the 
paresthesia and serves as a means of localizing the tumor. 

sensory disturbances thus result prominently from implica- 
tion of the posterior spinal roots, so motor symptoms indicate the in- 
volvement of the anterior roots. Muscular spasm, twitching and con- 

'ure appear in parts of the body supplied with motor innervation 

from the same segments of the cord which supply the corresponding 

sory innervation. Tenderness and rigidity of the spine, abdominal 

pain and tenseness, in the limbs pain and contracture are thus seen 

n together. Hemiparesis, hemiparaplegia, paraplegia involving all 
four limbs may all appear in orderly succession. The Brown* 
Sequard paralysis with loss of motion and muscular sense on the side 
of the lesion and loss of the cutaneous sense, especially pain and tem- 
perature, on the opposite side is rather a frequent incident of spinal 
tumor. It is never pronounced, however, soon disappears and occurs 
only when the tumor is above the lumbar region. Jf the tumor is 
in the latter region the reflexes may be lost, but when it is in the cer- 
vical region they will be exaggerated. The electrical excitability of 
tin- affected muscles undergoes alteration on account of tin- degener- 
ation in the anterior roots. Atrophy of the muscles ma) occur, espe- 
cially in the legs, from the same, cause. 

Vasomotor symptoms, involvement of the bladder and rectal func- 
tions, and later on intractable bedsores may all be observed. Dilata 
tion and contraction of the pupils are observed in high cervical tun 

When the cauda equina is the scat of a m<»rbid growth there is pel 
vie pain, especially in tin anal and perinea] region, and out along the 
Ataxia. 1<>^ «>f the kne< and paralysis of the blad- 

der may be seen. 

From this description it will be readil) son that no absolutely 
uniform clinical picture can be drawn to fit all cases alike. < >nlv a t: 
OUgh knowledge of the anatomy and physiology of the 11 enable 

the physician t«. appreciat< mosl clearly the pn I a tumor. The 

symptoms must be studied alwa; her: the entire picture | 

sented by tin- case must be looked at in toto; and while under ob 






560 



THE NON-NEURONIC DISEASES 



tion every change in the symptomatology must be carefully noted, cor- 
related carefully with what precedes and follows it, and compared with 
the normal functions of the cord. As the lesion is a changing one, the 
cause of the symptoms will undergo variations. 

In regard to the symptomatic diagnosis of the location of the 
tumor the reader is referred to the chapter in the earlier part of the 
book devoted to spinal localization. The careful determination of the 
limits of the anaesthesia affords the best guide, and next to this -the 
muscles that may be paralyzed. These should then be compared with 
the table of spinal functions reproduced in an earlier chapter. As a 
rule the tumor is located from two to four inches above the upper- 
most border of the area of anaesthesia. Spinal sensitiveness may also 
help slightly to localize the tumor. The peripheral neuralgic pain, if 
sufficiently constant and localized in the area of a nerve distribution, 
may assist by leading back to the corresponding nerve-root. Unfor- 
tunately, however, pain is far too diffuse a symptom to be of much aid. 

Diagnosis. — This is much more difficult than in brain tumor, for 
the reason that there is a wider variability in the symptomatology. 
Note should be carefully taken of the signs indicating gradual, pro- 
gressive compression of the cord and nerve-roots. The pain and its 
special character, the progressive paralysis, the rigidity of the spine, 
the muscular contractions in the limbs, the early and marked exaggera- 
tion of the reflexes of the leg, the extension of the symptoms from one 
side to the other, and the possible existence of metastatic conditions of 
similar import in other parts of the body, such as syphilis, tubercu- 
losis, multiple sarcomata and neuromata, are all suggestive of a spinal 
neoplasm. 

Caries of the spine is to be differentiated from tumor by the ab- 
sence, or less severity, of the root signs, by the lesser degree of paraly- 
sis, by the presence of bone disease with external tumor or kyphosis, 
by pain upon movement, the age of the patient and the existence of 
the tubercular diathesis. 

The symptoms of hypertrophic pachymeningitis are bilateral from 
the beginning, and represent a much more extensive lesion longitu- 
dinally in the cord. The sensory symptoms in the arms are more 
marked and there is more often early and limited anaesthesia. The 
distinction between this form of meningitis and cervical tumor, how- 
ever, is at times extremely difficult and for obvious reasons. Menin- 
gitis is often a part of the symptom-complex of tumor. 

In transverse myelitis the pains are not so severe and radiating, 
but there is more of a girdle phenomenon. The trouble does not pro- 
gress and exhibit, like tumor, the intense initial pains, followed by 
motor paralysis and anaesthesia and the signs of more or less definite 
localization. Here again, however, a differentiation is often difficult 
because myelitis is one of the secondary effects of tumor. Occasion- 
ally the cause of such an obtrusive myelitis can be discovered to be a 
tumor, by the manifestations and history of the case, before the appear- 
ance of the myelitic symptoms. 

Neuralgia of special nerves ought not to give much trouble in 
the differential diagnosis for it is distinctly unilateral, limited to the 



THE NON-NEURONIC DISEASES 561 

nerve involved, and is devoid of the motor and spinal symptoms of 
tumor. 

Skiagraphy should always be kept in mind as a possible means 
of diagnosing and locating some of the spinal tumors. 

Prognosis. — Except in syphilitic cases the prognosis of spinal 
tumor is bad. The course and duration of the trouble depend very 
largely upon the character, size, and location of the neoplasm. Most 
cases run from three to five years, two or three years being the aver- 
age. Tubercles have been known to cease growing. All other forms 
of tumor continue, as a rule, to steadily progress. Rapid increase of 
symptoms and stationary periods often alternate in the course of the 
disease. Even transient improvement may awaken false hopes. 
Syphilomata are the only growths that are amenable to medicinal in- 
fluence, and even these, if long neglected, offer an insurmountable re- 
sistance. In a few other types of tumor lives have been saved bv 
surgical intervention. Death is caused by exhaustion, bedsores and 
all the usual sequelae of a severe meningomyelitis of a high degree. 

Treatment. — There is only one form of spinal tumor that is 
directly amenable to medicinal treatment, and that is syphiloma ; and 
in this form the results are usually in inverse ratio to the length of 
time the trouble has existed, and the destructive damage already done 
to the cord. Therefore the earlier the treatment is instituted the bet- 
ter will be the results. It is a good rule, unless the indications point 
absolutely away from syphilis, to put every case of spinal tumor upon 
a trial antisyphilitic treatment. This is especially advisable if there 
has been exposure and a possibility of infection. The frequently evanes- 
cent character of the primary and secondary manifestations in cases 
of tertiary syphilis, may give ground for the denial honestly on the 
part of the patient that he has the disease. If he admits circumstances 
by which the disease may have been acquired, a most thorough course 
of antisyphilitic medication should at once be begun and tried for a 
while. It cannot do the slightest harm, should the tumor be of any 
other nature than syphilitic, and it may. in case it is the latter, save 
the patient's life. Of course when there is a clear history of infection. 
the treatment should not be delayed a moment. A day or two delay 
may eventuate in irreparable damage to the cord. The treatment 
should be both prompt and vigorous. Increasing doses of the Iodide 
<»f potassium, from sixty grains a day on up. should be started, just 
as I have recommended in the chapter on syphilis of the nervous sys- 
tem. If in a few days there is no marked change in the symptoms 
mercurial enunctions had better be added to the treatment. In some 
old cases, known to be syphilitic, the treatment just suggested may 
fail to modify the symptoms. In these cases tin- changes in the cord 
are beyond all human means of repair. 

Most of the other forms of tumor suggest the possible interven 
tion of surgery but their medicinal treatment does not extend beyond 
the administration of tonics and remedies for the symptoms. \ tuber- 
culous condition may call for tonics, iodine, oleum morrhuae, hut not 
much direct effect will he thus exerted upon the spinal tubercle. The 
same mav be said of the use of arsenic and nitrate of silver in glioma 






56: 



THE NON-NEURONIC DISEASES 



and sarcoma. The iodides are often despairingly tried in all cases, 
with the vague idea of causing absorption of the growth. The idea is 
as poorly founded as the results will undoubtedly be. 

Surgery should always be considered, not merely as a last resort 
but as offering in some cases a positively hopeful outlook. While the 
general results are not brilliant, in individual cases some splendid re- 
turns have been secured. In capable hands the operation is not now 
so dangerous as it used to be. Even an exploratory operation is to be 
commended where so desperate a disease is under consideration and 
there is doubt, leaning, however, towards the diagnosis of tumor. The 
extra-dural tumors are of course the most favorable for operation, 
though even the unfavorable intra-medullary growths may be wisely 
enucleated if they are single and of recent development. According to 
Gowers and Horsley, who led the way to the surgical treatment of 
these tumors with their first brilliant case, almost all intra-dural tu- 
mors are operable. Multiple, metastatic and advanced medullary tumors 
are beyond all aid, and therefore should not be subjected to the knife. 

The diagnosis of the location of the tumor must be very definite 
before an operation is undertaken. In most cases the tendency is to 
locate the tumor too low in relation to the guiding symptoms. In Gow- 
ers and Horsley's first case, the tumor was higher than the symptoms 
suggested, four inches above the level of the pains and anaesthesia. 
According to Bruns, generally only the segmental height of the upper 
border of the tumor can be determined. The highest point of the 
sensory, motor and painful manifestations should be carefully estab- 
lished and this compared with the known physiological functions of the 
various segments of the cord. The chapter on spinal localization and 
topical anatomy of the cord can be consulted for further details. The 
Rontgen ray is a modern means of great value in some cases for 
locating the tumor and should always be resorted to to add if possible 
further confirmation to what may be nevertheless an almost positive 
topical diagnosis. 

In all cases, operable or inoperable, the pains will have to be 
controlled, bedsores will have to be guarded against and properly 
treated when present, disease of the bladder will need attention and 
other symptoms, complications and sequela? will have to be continu- 
ally looked to. The management of a case of spinal tumor is never a 
very grateful task. 



CAVITIES OF THE SPINAL CORD. 

The formation of cavities within the spinal cord is intimately re- 
lated to the presence of gliomatous tumors. They are the result of 
congenital defects. The cavity may appear as a primary defect and 
be the only abnormality present. This is hydromyelia and is homolo- 
gous with hydrocephalus. Gliomatous tumors may form within the 
spinal cord, become absorbed and thus leave a cavity, or gliosis may 
take place in the walls of a congenital cavity, enlarge into a tumor 
distending and deforming the original cavity and then undergo partial 
or complete absorption, thus leaving a cyst but one somewhat differ- 



THE NON-NEUBON1C DISEASES 563 

ent in shape from the original. This is known as syringomyelia. 
Finally, the remains of old hemorrhages and foci of inflammation may 
undergo partial resorption and leave small cavities. These may or 
mav not be congenital. These myelitic and hemorrhagic remains may 
be traumatic in origin or may accompany hydromyelia and gliosis. For 
the sake of convenience then, the cavities of the cord may be discussed 
under the three heads, (a) Hydromyelia, (b) gliosis and syringomyelia 
and (c) myelitic and hemorrhagic excavations. 

Hydromyelia is primarily a dilatation of the cord, especially of 
the central canal. It is lined therefore with epithelium. It is of the 
nature of a developmental defect and may be associated with hydro- 
cephalus and spina bifida or exist alone. It is an anatomical curiosity 
without clinical importance. As a rule it only presents symptoms when 
gliosis or gliomatosis takes place within its walls and it becomes occu- 
pied by a growing tumor. Then it becomes clinically interesting. 

Gliosis and Syringomyelia. — Many believe that this and hydro- 
myelia are identical conditions primarily. The hydromeylia of child- 
hood evolves in the course of time and from various factors into the 
syringomyelia of adults. As syringomyelia develops behind the cen- 
tral canal, and sometimes around it, it is not always a mere modified 
hydromyelia. It is a posterior spinal defect of development. In most 
cases it is a persistent patulency of the anterior portion of the posterior 
limb of the primitive developmental sulcus. 

Etiology. — Typical syringomyelia, as I have intimated, is a con- 
genital trouble associated with or following a gliomatous neoplasm. 
Dana says it is more frequent than amyotrophic lateral sclerosis but 
less frequent than multiple sclerosis. It is far more common in men 
than in women. In Schlesinger's 190 cases, 133 were men, 57 women. 
Most of the cases begin prior to the thirtieth year ; usually about the 
age of twenty or twenty-five. It is commonly affirmed that heredity 
does not constitute an etiological factor in this disease, and yet three 
members in the same family have fallen victims to it. In the non- 
gliomatous, traumatic syringomyelias there is believed to exist an in- 
herited or congenital predisposition on account of which the trauma 
operates in the way that it does. The disease cannot be connected 
with alcoholism, syphilis or dissipation. It has followed pregnancy and 
certain infectious diseases. Dana observes that it seems to occur to a 
large extent among those who follow manual occupations, such as 
butchers, tailors, etc. I observed it in a man who after recovery from 
influenza went to work in the fields and daily plunged into cold water 
while he was hot and perspiring. Oppenheim says that spinal cavities 
have often been observed in syphilitic individuals and accompanying 
Other disease of the cord. These cases are not typical, however, as 
are the non-syphilitic gliomatous cases. 

Pathology and Pathogenesis. — Upon taking tin- cord out of 
the spinal canal nothing abnormal may appear about it. Tt may seem 

a little larger in some places, softer than normal, and fluctuating. The 
essential finding of the disease is only observed when the cord is cut 
across transversely. At once a carcmous formation is seen in the gray 
matter. Tt usually occupies the center of the cord, obliterating and 



564 



THE NON-NEURONIC DISEASES 




FIGURE 122. 




FIGURE 123. 




FIGURE 124. 



Figure 122, Hydromyclia of upper dorsal cord. Figures 123 and 124, Syringo- 
myelia. Sections made in upper and middle cervical cord. (Striimpell — Jakob.) 



THE NON-NEURONIC DISEASES 565 

including the central canal. It may extend in the lateral gray mat- 
ter or into the horns, especially the posterior horns. In the latter it 
has been seen to reach almost to the edge of the cord. The white 
matter is not touched by it. The shape of the cavity is irregular and 
various. It may be angular, round, oval, stellate, diamond or any 
imaginable shape. It is most frequently seen in the cervical part of 
the cord, though it may be in any part, or even extend throughout its 
entire length. The bore of the cavity when thus extended is never 
perfectly uniform. There are apt to be here and there wide lacuna 
with narrow connecting channels. Lining the cavity is a well-formed 
membrane and around it a layer of gliomatous tissue. In some places 
this gliomatous tissue is proliferated and extends into the lumen of 
the cavity. Occasionally it may be seen to occupy the whole cavity 
and even be distending it. The primitive ciliated epithelium of the 
original central canal may be noted here and there on the cavity wall. 
The cells of the gliomatous tumor are seen to be in various stages of 
formation and decay. Hemorrhagic and inflammatory foci may be 
observed in certain cases. In some cases other developmental defects 
have been observed outside of the cord. Thus the brain has revealed an 
internal hydrocephalus and the cerebellum has been absent. Tumors, 
probably gliomatous, have also been seen in the pons, the cauda 
equina and elsewhere, showing that the gliomatous growths of the 
cord proper constitute but a part of a widespread pathological tendency. 

The original cause of these cavities is a congenital, developmental 
defect in the posterior part of the spinal cord. There is a defective 
closure of the central canal and posterior septum, with the remains 
of epiblastic tissue in the walls of the imperfect closure. Just to 
what extent the entire syringomyelic formation is congenital in its 
origin is not easy to determine ; nor can it be stated positively just how 
much it has been enlarged and altered by the over-growth and sub- 
sequent degeneration of the gliomatous tissue. The process of cavity 
formation is thus a complicated one, always primarily congenital or 
hydromyelic, but secondarily enlarged and distorted by the intra- 
cavernous growth and degeneration of a neuroglia tumor. 

The primitive furrow in the embryo deepens, its sides rise up, 
arch inward, coalesce, and thus transform it into a tube. At about 
the sixth week this central canal is comparatively very large, is dia- 
mond shaped and reaches from the anterior to the posterior surface of 
the cord, its walls are thinner in front and behind than they are at 
the sides. As the posterior columns develop, the posterior part of this 
canal becomes narrow and elongated, almost to the point of being a 
mere fissure. The surrounding structure consists of embryonal cells 
which afterward are transformed into the proper nerve elements. 
Finally the canal becomes divided into an anterior and a posterior por- 
tion. The former ultimately constitutes the permanent central canal. 
the sides of the posterior coalesce and form the posterior septum. 
When either of these divisions of the primitive central canal fail to 
close properly, there is a surplus of the embryonal epiblastic tissue 
present which is very liable later on to undergo hyperplasia and tumor 
formation. The cells are small, round or irregular in shape, with large 






566 THE NON-NEURONIC DISEASES 

nuclei and numerous fine fibrillary prolongations. Bloodvessels pene- 
trate these gliomatous growths and being diseased rupture and leave 
hemorrhagic debris. The tumors themselves are very prone to degen- 
eration and disintegration, transforming an originally limited cavity 
into a much more extensive one. The disintegration and disappearance 
of the gliomatous tumor are due, in a measure, to the liquefactive de- 
generation of the glia cells. The oedema of the cord may be partly re- 
sponsible for and partly the result of this. 

Symptoms. — Some cases of syringomyelia do not seem to produce 
any symptoms and they are only discovered upon post mortem examina- 
tion. It is probable they are cases of hydromyelia in which no gliosis 
has taken place. The latter process in the majority of cases probably 
begins spontaneously, though in some cases it would not occur at all 
if there had not been some exciting initiative cause, like trauma, hem- 
orrhage, meningitis, etc. 

The symptoms of syringomyelia are the result of the 'pressure 
and destruction of gray matter caused by the tumor. This explains 
why the infantile form of the trouble is without clinical manifestation 
generally, whereas the adult form almost always exhibits outward signs. 

The clinical picture of the disease is subject to wide variations. 
This would naturally be expected from so variable and extensive a 
lesion. The establishment of types of the disease, such as Schlesinger 
and others have made, seems to me to be arbitrary, burdensome and 
dangerously suggestive of the types being different diseases dependent 
upon different lesions. The only anatomical basis for the separation 
of these types is the accidental location of the pressure and destructive 
influences within the cord. Hence while the clinical features are in a 
way complex, it is not due to the complexity of the disease but to the 
complexity of the physiological functions of the cord and their dis- 
turbance by the particular location of the disease process. 

As the cavity usually appears first, and is most extensive in the 
cervical part of the cord the symptoms appear most prominently in 
the upper part of the chest, the lower part of the neck, in the shoulders, 
arms, and hands. 

Perhaps the most striking symptom, due doubtless to the destruc- 
tion of the gray matter of the central cord, is the progressive muscu- 
lar atrophy. It usually begins in the hands, sometimes in the shoul- 
ders and upper arms. Sometimes it develops in the legs. It is a true 
atrophy and is liable to be mistaken for the ordinary form of spinal 
progressive muscular atrophy. The smaller muscles of the hand waste 
first and the main-en- griff e, or claw-hand, develops. The muscles on 
the back of the scapulae, the deltoid, the biceps and triceps, diminish 
in size. The wasting is usually bilateral and is accompanied by a 
fibrillary tremor. There is a partial reaction of degeneration and dis- 
turbance of the reflexes. Weakness and paresis proceed, pari passu. 
with muscular wasting. In the legs', which are usually affected later, 
there is atrophy with more or less spastic paraplegia; in other words a 
condition resembling amyotrophic lateral sclerosis, and probably pro- 
duced by the same sort of a disease process. The face and throat mus- 
cles are not often affected and the sphincters remain intact. On ac- 



THE NON-NEUBONIC DISEASES 56? 

count of the unequal wasting of the muscles of the back spinal curva- 
tures occur, especially scoliosis. The drooping of the scapula and the 
lessening of the shoulder joint cause unilateral deformities often about 
the shoulder. 

The sensory disturbances are unique and almost pathognomonic. 
There is a dissociation between the tactile and pain senses, a simple 
analgesia without anccsthesia or hyperesthesia. The temperature sense, 
like the pain sense, is also lost. A hot iron and a piece of ice placed 
against the skin awaken only the sense of contact. With the iron hot 
enough to burn the skin, it still does not cause any distress. This 
explains the many scars and marks of traumatism so often carried by 
the patients about on their bodies. The exact anatomical basis for this 
remarkable symptom is not fully known. It is thought to be due to 
the destruction of the gray matter of the posterior commissure, through 
which course the fibres of Gowers' tract that carry the pain and heat 
impulses. In some instances the conducting functions of the cord for 
sensory impulses of all sorts are so profoundly damaged that wide 
areas of complete anaesthesia are observed. The Brown- Sequard type 
of hemianaesthesia is accordingly noted. Paresthesia is not infre- 
quent and in rare instances actual pain may be present. The special 
senses do not participate in the trouble. 

This dissociation of the tactile and pain sense, with the progres- 
sive muscular atrophy above and the amyotrophic sclerotic manifesta- 
tions below, constitute the pathognomonic picture of the disease. 

Other symptoms of great variety may also be looked for. Among 
these the vasomotor and trophic signs stand prominently forth. They 
must be distinguished of course from the mere injuries which these 
patients so often cause themselves on account of the absence of the 
pain and heat senses. CEdema, redness, sweating, slow-healing sores 
appear on the hands and arms. Eczema, bullae, herpetiform eruptions 
break out on the skin of the body. The latter is sometimes dry and 
leathery and unhealthy looking. Whitlows occur on the fingers, and 
the nails become brittle and fall out. In about ten per cent, of the 
cases arthropathies occur. The bones become fragile and necrosed, 
and ankyloses take place in the joints. Spontaneous fractures are not 
to be forgotten as unfortunate possibilities. The mutilations, scars, 
deformities often render these poor creatures a sorry sight. 

Inequality of the pupils, and iater on distinct bulbar symptoms 
with implication also of the rectal, vesical and sexual functions show 
the gradual and progressive extension of the lesion. 

Many changes may be rung upon the above more or less typical 
clinical picture, and some novel combinations in the symptomatology 
make their appearance. These are not types of the disease, but mere 
atypical presentations of the symptoms. Morvan, for instance, de- 
scribed what he supposed was a new disease, but which is now acknowl- 
edged to be hut a particular presentation Of syringomyelia. In the eases 
that Morvan described, analgesia, thermo-anaesthesia, tactile anaesthesia, 
muscular atrophy and felons on the fingers all occurred. 

A rare group of symptoms thai have been separately seen in differ- 
ent cases are facial hemiatrophy, anaesthesia of the trigeminal region, 



5 68 



THE XOX-XEURONIC DISEASES 




early bulbar phenomena, cranial nerve palsy, nystagmus and mellituria. 
A sharp limitation of the symptoms may be due to the confinement of 
the gliosis to the posterior or anterior horns of one side. In three cases 
Oppenheim observed the disease to be restricted to the lower limbs in 
the beginning. I saw a case in which in the beginning there was pain in 
the left hip, passing down the leg and followed by a very slight degree 
of atrophy, oedema and changes in the joints. Later on the pain ceased 
in the leg and marked atrophy appeared in both shoulders, in the back 
muscles and muscles of the scapulae, and part way down the muscles of 
the arm. Arthropathies were marked in the knee of the left side and 
shoulder joints. The other symptoms, trophic and sensory, were not 
unusual. 

Optic neuritis and choked disc have been seen, and some still 
maintain that in part, at least, the symptom-complex of Morvaris dis- 
ease is due to a complicating peripheral neuritis. 

If there is involvement especially of the posterior tracts, the disease 
may asume the complexion of tabes dorsalis. 

Diagnosis. — Progressive muscular atrophy, dissociation of the 
sensory symptoms, general vasomotor and trophic symptoms, the amyo- 
trophic lateral sclerosis symptomatology in the lower limbs and spinal 
curvature constitute the decisive indications of syringomyelia. The 
numerous atypical combinations and presentations of its symptoms may 
easily delude one into mistaking it for some other disease. This was 
much more common in the past than it is to-day, and we now recognize 
that there were named and described niany separate affections that were 
really instances of syringomyelia. 

Both ordinary progressive muscular atrophy and amyotrophic lat- 
eral sclerosis are very liable to be mistaken for it. The former is de- 
void of sensory symptoms entirely, and the latter is not characterized 
by flaccid atrophic paralysis with preservation or diminution of the 
knee-jerks. The sensory phenomenon when present will indicate con- 
clusively syringomyelia. 

Hypertrophic cervical pachymeningitis causes muscular wasting, 
sensory loss and other resemblances to syringomyelia. It may be dif- 
ferentiated, however, by the local spinal tenderness, the spinal root 
symptoms, the lesser extent of the anaesthesia in relation to the wasting 
and the absence of the characteristic indications of the cord disease. 

Chronic transverse myelitis should give no very great trouble in the 
diagnosis. 

Caries of the spine, with atrophy, sensory disturbances and 
pupillary changes, is nevertheless separated by the history of tubercu- 
losis and disease of the vertebrae. 

Gliosis and glioma of the cord are two separate conditions, accord- 
ing to Hoffmann. The former is a rapid, the latter a slow process. 
They are not necessarily syringomyelic. 

Various peripheral nerve diseases may be confused with syringo- 
myelia. Morvan's disease does not call for a differential diagnosis, as 
it is syringomyelia with possibly a complicating neuritis. It is the form 
of syringomyelia that is most likely to be confused with aincsthctic lep- 
rosy. The detection in the skin of the lepra bacillus is, of course, final. 



THE XOX-XEUROXIC DISEASES 5O9 

In leprosy the cutaneous evidences are in plaques, including the face 
and lower limbs as much as the arms. There is no dissociation of the 
sensory symptoms as in syringomyelia, but the sensory phenomena fol- 
low the innervation particularly of the peripheral nerves. In leprosy 
the amyotrophic paraplegia of the lower extremities, the bulbar symp- 
toms, the nystagmus sometimes seen in syringomyelia are wanting. 

Neuritis of the brachial plexus has all the earmarks of peripheral 
neuritis and very few of those of the spinal cord cavity. 

Hematomyelia has its own clinical manifestation, though it may 
later on develop into a syringomyelia. 

Hysteria, Raynaud's disease, acroparesthesia are easily distin- 
guishable from the affection under consideration if emphasis is laid 
upon the characteristic symptoms of each respectively. 

Prognosis. — In regard to recovery this is bad. The disease is a 
progressive and congenital one. Periods of temporary cessation and 
even remissions occur. It ma}^ continue to advance for many years. It 
is doubtful if the case with lues, reported as cured under the use of 
potassium iodide, was typical. Death occurs from exhaustion, blood- 
poisoning and bedsores. 

Treatment. — This is of no avail and for reasons that are quite 
obvious. Warn the patient against injuring himself; maintain the 
nutrition of the muscles as far as possible by massage and electricity; 
administer general tonics ; and try, if you are in a hopeful state of 
mind, arsenic or silver nitrate. Lumbar puncture entertains the sur- 
geons without in the least helping the patient, and the finding of some 
drug or serum that will check the gliomatosis is a dream the realiza- 
tion of which is more to be hoped for than actually anticipated. 

Myelitic and Hemorrhagic Cavities. — The names of these suffi- 
ciently indicate their nature. They may occur alone or with typical 
syringomyelia. They are not large, are apt to be multiple and are gen- 
erally lined with connective tissue. 

SPINA BIFIDA AND OTHER CONGENITAL MALFORMA- 
TIONS OF THE CORD AND ITS MEMBRANES. 

Spina Bifida or rachischisis is an embryonal defect depending upon 
a failure of the spinal canal to close. It belongs to the same class of 
troubles as hare-lip, cleft palate and exstrophy of the bladder. The bony 
canal being open behind, the contents protrude under the skin and pro- 
duce a tumor, varying j n size from a nut to a child's head. The lum- 
bar region is its most frequent site. In some cases only the membranes, 
filled with cerebrospinal fluid, protrude. This is a meningocele. Some- 
times the cord protrudes with the membranes, giving rise to a myelocele 
or meningomyelocele. When the cord is syringomyelic, as it occasion- 
ally is, the cavities inside and outside of the cord form one and thus is 
established a syringomyelocele. The simple meningoceles and meningo- 
myeloceles are the most common and are sometimes called hydrorrhachis 
externa. When the cord and nerves are in the sac. they lie on the 
posterior, median surface. The lining of the sac is, of course, the dura 
and the subdural arachnoid. Outside of it the skin is usually normal. 




57o 



THE NON-NEURONIC DISEASES 



thin and covered somewhat with hair. The tumor itself is elastic and 
fluctuating. Pressure upon it has caused unconsciousness and other 
cranial disturbances. 

Other developmental anomalies and signs of degeneracy are often 
seen in these patients. They are usually mentally defective and are 
feeble, badly nourished and badly developed individuals. 

In simple meningocele, the cord being intact, there are often no 
special neurological symptoms. In the myeloceles, however, there is 
usually complete paraplegia, with muscular atrophy, more or less an- 
aesthesia, bladder and rectal trouble, diminution of the knee-jerks and 
the paralytic type of talipes, especially pes varus. Very few cases live 
to old age. The prognosis is always grave, with or without treatment. 

The treatment is entirely surgical. Unless hydrocephalus is pres- 
ent, extirpation of the sac may be attempted. The results are not very 
encouraging. Morton's fluid, consisting of iodine gr. x, potassium iodide 
gr. xxx, glycerin §j, has been injected into the cyst in oj quantities. The 
injection should be made at the side of the sac and the child be kept 
still. There is nothing to be gained by simple puncture and with- 
drawal of the fluid. It is a dangerous procedure. Only several months 
after birth should surgical intervention be thought of. 

MALFORMATIONS. 

There are certain malformations of the spinal cord that are only 
of anatomical and pathological interest. Such is amyelia or absence of 
the cord. It is morphologically and biologically interesting that when- 
ever the cord is thus wanting the brain also is wanting, but that oc- 
casionally the brain may be absent without the absence of the cord. 
In these cases of amyelia the spinal nerves are present and their inner 
roots swing loosely in the spinal cavity. These monsters, who, of 
course, never live, demonstrate most clearly that the nerves are not 
intrinsically developments of, or parts of, the cord, and that the brain 
is practically a hyper-development of certain anterior segments whose 
homologues are the segments of the so-called spinal cord. An atelo- 
myclia is the failure of development of a certain segment. When the 
cord is bifurcated, the condition is spoken of as diastcmatomydia. 
Rarely is the whole cord involved in this condition. Sometimes the 
cord is asymmetrical. A double cord, with two central canals, lying 
side by side, is known as a diplomyelia. None of these are of any 
clinical interest, but as indications of development and biological evo- 
lution of this part of the nervous system they are of entrancing interest. 
Micromyelia is an abnormally small cord. Van Giesen's heterotopia is 
an abnormally situated mass of gray matter. In most cases it is a 
post-mortem artefact. 

CAISSON DISEASE. 

This is sometimes called diver's paralysis and compressed air dis- 
ease. It is probably an affection of the entire nervous system or cerebro- 
spinal axis, though it is usually discussed as a spinal cord trouble be- 
cause its symptoms are largely paraplegic in character, and what few 



THE NON-NEURONIC DISEASES 5/1 

lesions have been found after death were seen in the cord. As diver's 
palsy the disease has doubtless long been known. In these modem 
davs of industrial activity and great engineering projects, with their 
mining, bridge-building and harbor construction, in which caissoiis 
filled with compressed air under water are made use of, the trouble has 
become more frequent and awakened a corresponding interest. Much 
study has been made of it. both clinically and experimentally, so that 
the literature is of no mean proportions. 

Etiology. — The essential cause of the disease is the high atmos- 
pheric pressure which the victims must perforce undergo in their occu- 
pation. It is therefore an acute disease with one specific cause, and 
all such factors as age. sex. race, etc., are of no significance, except so 
far as they are determined by the occupation. Those who work in 
caissons, bells and diver's apparatuses are usually subjected to a com- 
pression of from one to four atmospheres, which means from fifteen to 
sixty pounds to the square inch. When they emerge from the apparatus 
and the compression is withdrawn the symptoms of the disease make 
their first appearance. The differences in individual susceptibility may 
explain why, under the same conditions, some are affected while others 
escape. Every indication points to the mechanical pressure, rather 
than to any chemical or other change in the air, as the primary and 
essential cause of the disease. 

Pathology and Pathogenesis. — Xot many post-mortem exam- 
inations after diver's palsy have been made and our knowledge of its 
pathological anatomy, if it has any, is meagre. Most of the changes 
have been found in the thoracic part of the cord. They have consisted 
of numerous minute foci of hemorrhage and small patches of necro- 
biosis. Sometimes signs of an acute myelitis, disseminated myelitis, 
were noted. There were also slight fissures and ruptures. Changes in 
the brain have not been reported, though in a few cases the symp- 
tomatology was clearly that of cerebral apoplexy. 

On account of the scarcity of these post-mortem evidences, all ex- 
planations of the disease are to be taken somewhat tentatively. 

Perhaps the grossest explanation is that the increased pressure 
upon the surface of the body drives the blood inward and that whereas 
the other viscera are able to accommodate themselves to the congestion 
thus caused, the brain and spinal cord being encased in a firm, bony 
b ix, are not able to accommodate themselves quickly enough to the 
new state of affairs. A. II. Smith is the leading exponent of this view. 
There are many objections to it. however. The first is that the symp- 
toms appear not when the C '.need, but when it is re- 
lieved : not when the man is under the increased pressure, but when 
he comes out from it. It is a little contradictor} to declare that con- 
tion and minute hemorrhages, presumably produced while the man 
is being subjected to the exalted pressure, should produce no symptoms 
until he emerges from the caisson and the congestion and other sup- 
posed circulatory disturbances are relieved. Symptoms and k - 
must be synchronous or we must adopt the idea that the evi- 
dences of congestion are only manifested when the congestion is 
undergoing reduction. The illogicality of this, it seems to me. is an 



LI II 



572 THE NON-NEURONIC DISEASES 

argument against the congestion theory. The theory, moreover, upsets 
the long-taught physiological fact that on account of their rich anas- 
tomotic blood supply, both the brain and cord, above all the viscera, 
are protected from sudden and external circulatory disturbances of 
a purely mechanical nature. And finally, it does not harmonize with 
the localization of the chief center of the trouble in the dorsal region 
of the cord. Gowers suggests that the trouble is primarily due to the 
revulsive anaemia following the congestion, and that a nutritional dis- 
turbance, especially in that part of the cord which is so liable to nutri- 
tional disturbances, the dorsal region, is the immediate source of the 
paraplegia. 

Snell's hypothesis that it is due to the bad ventilation of the caisson, 
and the escape of carbon dioxide and oxygen into the blood-vessels and 
into the tissues, needs yet to be confirmed. 

The explanation that at present seems to have the strongest ex- 
perimental and pathological support is one in which it is affirmed that 
there is a sudden effervescence of gas in the blood and tissue juices. 
In this way the peculiar character and course of the symptoms, and the 
few pathological findings that have been noted, such as the spinal 
fissures and lacerations, the minute hemorrhages and spots of necrobio- 
sis from air emboli, are thought to be caused. The inflammatory 
changes are secondary results. Paul Bert was the first to suggest this 
theory, though Hoppe, Francois, Rameau and Baequay had previously 
surmised it. After recently experimenting upon animals, Hill and 
Macleod believe they have confirmed Bert's conclusions. In their sum- 
ming up, these investigators say that the circulation is not affected 
mechanically by compressed air. The cause of the disease is the escape 
of gas bubbles in the blood-vessels and tissue fluids upon the withdrawal 
of the compression. All of the fluids of the body generally effervesce 
somewhat after the manner of an opened bottle of soda water. The 
symptoms vary because the seats of the air emboli vary. 

Symptoms. — After a pressure of three or more atmospheres, the 
symptoms appear in those affected usually after the change is made 
from the high to the low pressure, especially if the change is made 
quickly. The individual must have been subjected to the pressure for 
at least an hour, and it usually is noted that the first signs of the dis- 
ease show themselves from, half an hour to an hour after he returns to 
the lower pressure. He may not have reached the normal atmosphere 
even before their appearance. 

There is first sadden pain in the limbs and joints, quickly followed 
by powerlessness and complete paraplegia. Not often are the arms 
involved. The pain, sharp and neuralgic in character, may appear in 
the epigastrium. These pains are often paroxysmal and are accom- 
panied by nausea and vomiting. Sometimes the legs are tender to the 
touch and the gait, when not completely paraplegic, is stiff anil awk- 
ward. Cephalalgia and dizziness are frequent. In the severest cases 
there is complete paralysis of both motion and sensation, involving legs, 
arms and trunk. In a few rare instances there have been seen hemi- 
plegia, monoplegia and other symptoms suggestive of cerebral apoplexy. 
Rapid coma and death have taken place in these apoplectic cases. 



THE XOX-XEUROXIC DISEASES 573 

The sphincters are usually involved, and there may be retention or 
involuntary emission of urine, constipation and erections of the penis. 
Clonic contractions upon movement have occurred in the abdominal 
muscles. In the paraplegic cases that do not get well bedsores, cystitis 
and all the later signs of a transverse myelitis appear. 

Progxosis. — Mild cases usually get well ; severe cases usually die. 
The former may run a course of only a few hours, or one of many 
weeks and months. In the mildest cases the recovery is generally com- 
plete. In other cases the paraplegia becomes permanent. Most of 
these cases run a course and terminate as any case of transverse 
myelitis would. Cases with cerebral symptoms are usually fatal. 

Treatment. — Prophylaxis is obviously most important. A care- 
ful selection should be made as to the general age and physique of the 
men employed in caisson work. Only strong, young men should be 
accepted and they should accustom themselves to the conditions before 
fully entering upon their work. It is imperative that they be total 
abstainers and temperate in all their habits. It is well to test the men 
with low pressures first before engaging them. Hill and Macleod sug- 
gest that the choice men for the work are those who are small, spare 
and wiry, and from twenty to twenty-five years of age. Emergence 
from the atmosphere should be gradual and always slower than en- 
trance. The longer the shift the greater will be the saturation of the 
body fluids with gas and the slower should be therefore the decom- 
pressing process. The higher the pressure is, the shorter should be the 
shift and the slower and more gradual the emergence. Both the caisson 
and the decompression chamber should be thoroughly ventilated and 
maintained at a temperature of about 60 degrees F. After decompres- 
sion the men should remain quiet for an hour or so and be recompressed 
upon the slightest sign of sickness. By observing these precautions 
Hill and Macleod believe that work of this character can be carried on 
without loss of life at a depth even of two hundred feet or about seven 
atmospheres or +100 pounds' pressure. 

When the disease has appeared its treatment is entirely symp- 
tomatic. The intense pains will demand the use of morphine. A. H. 
Smith suggests the use of ergot. Oxygen inhalations and the use of 
compressed air have been recommended. The treatment in other re- 
spects differs in nowise from that of myelitis. 

DISEASES OF THE CAUDA EQUINA AND FILUM TER- 
MINALS. 

Some authors devote a special section to these diseases, because of 
the multiplicity of the nerve roots here closely grouped together. It 
seems to me that this is unnecessary, as any disease that attacks the 
cord above is liable to attack the cauda and iilum. Hemorrhages, 
syphilitic and other neoplasms, inflammations and traumatisms are 
among the lesions found in this lowermost part of the spinal canal. 
In the absence of cord segments, the symptomatology will correspond 
with that of spinal root disease. The extent and character of the lesion 



574 



THE NON-NEURONIC DISEASES 



will determine the extent and character of the symptoms. All of this 
is to be determined by a rigid comparison of the symptoms with what 
we know of spinal localization. In a word, the diagnosis of diseases in 
this part of the cord is a localization diagnosis, plus the special feature 
that the symptoms will be of the root variety, but of very wide extent 
because involving so many roots. Bilaterality is a strong characteristic 

FIGURE 125. 




Semidiagrammatic illustration to show the topographical relationship between 
the vertebrae, the canda and the conus. (After Raymond.) 



of the symptomatology, though not absolutely so. There are small,, 
focal lesions here as elsewhere. 

The accompanying diagrams from Raymond and Schultze will 
assist better than any long description in making a localization diag- 
nosis. 

The prognosis and results of operative treatment in this part of 
the spine are rather encouraging. 

Spinal Concussion is a term used by some writers for a class of 
spinal symptoms caused by a fall, a blow or a general concussion, such 



THE XOX-XEUROXIC DISEASES 



575 



as occurs in railway accidents, and supposed to be without any ana- 
tomical foundation. In my opinion, the statement "without any ana- 
tomical foundation" used by these authors in this connection is a logical 
self-contradiction and at once wipes out spinal concussion as a special 
and unique disease. The term is misleading and had better be dropped. 



FIGURE 126. 




LTvI 



A schematic representation of the vertebral column with the lower part of 
the cord and the ^cauda. A lesion at A and one at B will produce pretty nearly 
the same set of symptoms. (After Schultze.) 

What is meant by it is a traumatic neurosis, for a consideration of 
which the reader is referred to another chapter. Under it the cases that 
are not of the nature of traumatic neurosis are hemorrhages and other 
well-known organic troubles that need no further discussion than what 
I have alreadv devoted to them. 



576 



THE NON-NEURONIC DISEASES 



PART 



Non- Neuronic Diseases of the Peripheral Nerves. 



Anatomy and Physiology of the Nerves. — We have already seen in 
our studies of the neurone that the peripheral nerves are nothing but 
the processes of cells, collected together into bundles and supported and 
protected by certain non-neuronic elements. Therefore literally there 
are no such things as peripheral nerves in the sense of being a special 
structure. They are mere outgrowths, extensions, branches, arms, as it 
were, from the central cells. We must get rid entirely of the idea that 
the peripheral nervous system is, as it used to be taught in the older 
anatomy, a network of conducting fibres, or wires, so to speak, to con- 
duct impulses from one point to another. It is more than this. It is 
the outlying part of the central nervous system itself, its own branches 
and integral structure. This newer conception of the nature of the 
peripheral nerves is absolutely necessary to grasp, if one is to under- 
stand their diseases. Many of the changes in the peripheral nerves, 
as in many of the degenerative forms of peripheral neuritis, so-called, 
are but the expression of trouble in the cells of the anterior horns of 
the cord and of the posterior spinal ganglia. A nerve therefore should 
always be regarded as a mere part of the central apparatus and not in 
the least as an independent structure. As the nerves are intimately 
related to, or are parts of, the spinal cord elements, if we are to divide 
up the great, uniform and harmonious nervous apparatus into such 
artificial divisions as the brain, spinal cord and nerves, it will be appro- 
priate to discuss the diseases of the nerves immediately after the dis- 
cussion of the diseases of the spinal cord. 

Anatomy speaks of motor and sensory nerves. W T e have already 
noted that this is somewhat of an artificial distinction so far as the con- 
stituent neurones are concerned ; for the motility and sensation depend 
not upon the neurones per se, but upon the end-organs with which they 
are attached. 

The motor nerves are but the neuraxones of the neurones whose 
bodies are located in the anterior horns of the cord and motor cranial 
nuclei. They are motor because they stimulate muscles. 

The sensory nerves are merely the peripheral ends of the neurones 
whose bodies lie in the posterior spinal root-ganglia, or in the ganglia 
(petrosal, jugular, geniculate, Gasserian, etc.) found on the roots of the 
sensory cranial nerves, and whose central ends project into the cord and 
medulla. They carry impulses from the peripheral parts of the body 
to the central ganglia and are thus sensory in function. When these 
motor and sensory peripheral processes are bound together by con- 
nective tissue, in which course the minute nutrient blood-vessels and 
lymphatics, we have what is termed in gross anatomy a nerve. 

A transverse section of a nerve then presents an easily understood 
and typical picture. It is a bundle of smaller bundles, which smaller 



THE XOX-XEUROXIC DISEASES 



577 



bundles are made up of the central cell processes. The smaller bundles, 
called funiculi, are embedded in the perineurium which forms itself into 
concentric rings or laminae immediately around each funiculus, but 
whose fibres run in all directions between them. Around the outer 
edge of the nerve, where it is named the epineurium, it again assumes 
the ring-like arrangement. 

The perineurium is a connective tissue structure and contains the 
arteries, veins and lymphatics. It is therefore that part of the nerve 
that is capable of undergoing inflammation, hyperplastic new growths 
and other changes common to the vascular and connective-tissue ele- 
ments. The perineurium immediately around each funiculus sends 
septa, endoneurium. in various directions into it, which separate and 

FIGURE 127. 




— Transverse section of the sciatic nerve of a cat about x 100.— It consists of 
bundles {funiculi) of nerve-fibres ensheathed in a fibrous supporting capsule, epi- 
neurium, A , each bundle has a special sheath (not sufficiently marked out from the 
epmeunum in the figure) or perineurium B ; the nerve-fibres N/are separated from one 
another by endoneurium ; L, lymph spaces ; Ar, artery ; V, vein ; F, fat. Somewhat 
diagrammatic. (V. D. Harris.) 

support the nerve-fibrils, whose cut ends we can recognize in the little 
white circles, with a dot in the middle of each circle. Blood-vessels do 
not seem to penetrate the funiculi, but the endoneurium as well as the 
perineurium contains lymphatic tracts by which the fibrils are nour- 
ished. When a nerve sends off branches to unite with other nerves it 
is a funiculus that leaves the main trunk. The funiculi do not anasto- 
mose with each other in the same nerve trunk, nor do the branching 
fibrils emerge from the funiculi until they have reached their destina- 
tion. 

In its last analysis, a nerve fibril is seen to consist of an axis cylin- 
der surrounded by the medullary white substance of Schwann and the 
neurilemma. The axis cylinder consists of numerous minute strands 
running along side by side and representing the extension of the intra- 
cellular fibrous elements of the neurone. The medullary substance is 
seen to be absent or almost absent at various regular intervals along the 
course of the fibrils, so that the neurilemma is constricted and sinks 



578 



THE XOX-XEL T ROXIC DISEASES 



down close to the axis-cylinder. These constrictions in the fibril are 
known as the nodes of Ranvier. It is supposed that the nutrient sub- 

FIGURE 129. 



1 "A 



FIGURE 128. 



— A node of Ran- 
vier in a medullated 
nerve - fibre, viewed 
from above. The me- 
dullary sheath is inter- 
rupted, and the primi- 
tive sheath thickened. 
Copied from Axel Key 
and Retzius. x 750. 
(Kleinfc Noble Smith ) 



-Nerve- 
fibre stained 
•with osmic 
acid. A, node; 
B, nucleus. 
(Key and Ret- 
riiw.) 



stance enters the fibril here. At all events it is always at the nodes that 
the branches are given off by the fibril. In the white medullary sub- 






THE X0X-XLUR0X1C DISEASES 



579 



stance are to be seen numerous minute oblique lines. These are called. 
Lantermann's incisures. They probably represent breaks caused by the 
handling of the nerve. About midway in each inter-nodal space, and 
just beneath the neurilemma, is a nucleus. Non-medullated fibrils are 
.found in the olfactory and sympathetic nerves. The neurilemma is not 
found on the neuraxones making up the white substance of the brain 
and cord. 

There is nothing to be said of the physiology of the nerves beyond 
what has been said of the physiology of the neurones. 

General Pathology of the Peripheral Nerves. — It is clear from 
their anatomical structure that the nerves, like all parts of the nervous 



FIGURE 130. 



FIGURE 131. 




—Two nerve-fibres of 
sciatic nerve, a. Node of 
Ranvier. b. Axis-cylinder, 
c. Sheath of Schwann, with 
nuclei. Medullary sheath is 
not stained, x 300. (Klein 
and Noble Smith ) 



-Axis 
cylinder, high- 
ly magnified, 
showing its 
component 
fibrils. 
(M. Schultee.) 



system, may undergo both the degenerative and the inflammatory 
process. The former used to be called parenchymatous inflammation. 
In our previous study of the degeneration and regeneration of the 
neurone we noted that it was not an inflammatory process at all. The 
latter is still correctly referred to as an interstitial inflammation, for it 
is a true inflammatory process and involves the interstitial connective 
tissue and its vascular contents. When this interstitial tissue becomes. 
overgrown the nerve fibrillar are compressed and more or less degener- 
ated ; the nerve becomes hard ; and tin- whole condition takes the name 
<>f sclerosis. The degeneration thus caused in the true nerve-fibrils is a 
secondary phenomenon. 

It is still an open question whether a primary degeneration ever 
takes place in these peripheral nerve fibrils that is not dependent upon 
trouble in the cell-bodies and their nutrition. In certain toxic states 







5 8o 



THE NON-NEURONIC DISEASES 



we often find the peripheral nerve fibrils wasted, but no discoverable 
signs of inflammation to enable us to say the degeneration was sec- 
ondary, nor discoverable changes of a positive character in the related 
cell-bodies. The degeneration under such circumstances appears to be 
purely primary. Some investigators hold that the toxin has directly 
damaged the peripheral nerve-endings. They are few, however. Oth- 
ers maintain that it has affected the nutritive function of the central 
cells and so caused the degeneration in these remote parts of the neu- 
rones. When the damage to the central cells is obvious and mechanical, 
trie resulting deterioration in the peripheral nerve filaments is not a 
secondary degeneration. It is but a part of the degenerative process in 
the whole neurone. 

In primary degeneration I assume then that the entire neurone is 
affected ; that through hereditary or other influences the cell-body has 
lost its power of keeping up the nutrition of the processes, and as a 
result the latter waste. The peripheral degenerations observed in many 
hereditary diseases and in many toxic and infectious states are un- 
doubtedly of this character. Certain cachectic states in which there is 
especially disturbed nutrition, thus exhibit peripheral nerve degenera- 
tion. Diabetes is an example. Defective metabolism associated with 
lithaemic, anaemic and autointoxic conditions may be accompanied by 
the parenchymatous wasting in the nerves. 

In all of these conditions it seems to me very essential that we 
should regard the peripheral degeneration as a mere expression of 
a disturbance in the nutritive function of the central cell-bodies, and 
that this disturbance is the result of a much larger and more generalize;! 
disease process. In this sense primary degenerative processes, pure 
neuronic disease, in the peripheral nerves, is never any thing more than 
a collateral exhibition in another and more distinct disease. I empha- 
size this fact because upon it hang the prognosis and treatment of these 
peripheral degenerative manifestations that seem to be primary. I 
emphasize it also because it will serve to stimulate the practitioner to 
always look further than the nerves, when these are primarily de- 
generated, for a more profound and widespread disease involving the 
entire organism. The majority of the cases of toxic polyneuritis serve 
as apt illustrations of my point. 

The secondary degenerations, similar to the Wallerian degenera- 
tion that sometimes occurs in the peripheral nerves, result from trau- 
matic causes that compress, lacerate or sever the neurones, so that 
parts of them are separated from their nutritive cell-bodies. In this 
condition the distal or severed end of the neurone undergoes complete 
disappearance; the proximal end passes through a much slower, in- 
complete and at times scarcely noticeable retroactive degenerative 
process. It is presumed that here the whole neurone has been put out 
of service by the injury and that even the cellular end misses the normal 
stimulus ncessary to keep it up to its normal nutritive tone. As in all 
of these traumatic or secondary degenerations, the inflammatory phe- 
nomenon sooner or later makes its presence known, I will refer to them 
under the general head of neuritis. 






THE NON-NEURONIC DISEASES 58 1 

NEURITIS. 

An inflammation in a nerve begins, of course, in the interstitial or 
non-neuronic tissues. The nerve fibrillar are damaged secondarily. It 
may well be that the cause, compression for instance, may be just 
sufficient to initiate the degenerative process in the fibrillae before the 
inflammatory process in the interstitial tissue has gotten well under 
way. Under such circumstances the degeneration would be regarded 
as secondary, but not due to an associated inflammatory process. The 
distinction is not an important one, however, since it merely means that 
degeneration is quicker to occur than inflammation in the presence of 
the same active cause. As sooner or later in all such cases inflamma- 
tion does appear, it is convenient and not illogical to consider the two 
processes, inflammation and secondary degeneration, together. 

When the inflammatory process originates in and remains con- 
fined to the perineurium, the disease is called perineuritis. If the in- 
terstitial tissue is the seat of the trouble, it is known as interstitial 
neuritis. The parenchymatous neuritis of the older writers is a misno- 
mer, for, as I have shown, it is not inflammatory at all. It is a neural 
degeneration and exhibits all the changes seen in a secondary or Wal- 
lerian degeneration. It must be frankly admitted that these refinements 
of classification are of more pathological than clinical interest. We 
very rarely have a pure interstitial neuritis without secondary degenera- 
tion, or a secondary traumatic degeneration without an accompanying 
inflammation. Practically all cases exhibit the same symptoms. It is 
unfortunate that we cannot better distinguish the degenerative from 
the inflammatory trouble by the respective symptoms, for the prognosis 
of the case could be much more positively affirmed then. According to 
the relative amount and degree of the degeneration and inflammation, 

<mld the outlook of the case be bad or good. 

Etiology. — The causes of inflammation in a nerve are innumer- 
able. As a rule they can be classified under the three heads trauma, 
intoxication and infection. 

The traumatic causes include all factors by which the nerve is 
compressed, cut, torn, stretched or otherwise mechanically maltreated. 
< Obviously these causes may be severe or slight, limited or of wide 
extent, mediate or immediate. They may be rendered more destructive 
than they otherwise would be by a predisposing weakness caused by 
alcoholism, infection or other factor in the patient. To mention all of 
the ways a nerve may be compressed or lacerated would require a 
small-sized volume in itself. The nerves are exposed structures and 
therefore blows and contusions can easily reach them. So-called cratch- 
palsy, craft-paralysis, drunkard's paralysis caused by sleeping with the 
arm in a strained position under the head, are all due to pressure 
neuritis. Cuts and knife wounds are traumatic. Mechanical irritants 
like exce>>ive electric shocks, violent massage, direct blows near the 
nerve may easily cause it to become inflamed, especially in those pre- 
disposed by general debility. Inflamed swollen joints, neighboring 
tumor>. exostoses, dislocated and fractured bones are not infrequent 
causes. Tight bandages, excessive pressure in reducing a luxation, 



' 






582 THE NOX-N EURO NIC DISEASES 

wrenches, twists and nerve stretching of all sorts are to be reckoned 
with etiologically. Extremes of temperature are a prolific source, es- 
pecially when there is an underlying diathesis. In this way cold is a 
common cause of facial neuritis. Sometimes two or more causes act 
together. Sciatic neuritis may be due to the cold and pressure experi- 
enced in going to stool under special conditions. Corroding substances, 
acids, burns, scars and cicatricial compression are of the nature of 
traumata. Strains from overuse are often given credit for lighting up 
a neuritis, but they are hardly efficient as causes without the presence 
of an infection or vitiated state of the constitution. They are more of 
the nature of exciting causes. I have seen a neuritis start from lifting a 
child suddenly by one arm. Birth palsies, especially those that occur 
from instrumental delivery and abnormal presentations, are usually 
neuritic. Non-purulent ascending neuritis used to be much talked of 
by the older pathologists. Nowadays it is scarcely believed to occur. 
Only the purulent form really ascends a nerve. Neuritis may be caused 
by puncture of the nerve with a hypodermic needle, or the introduction 
of irritants like ether, perosmic acid, chloroform, etc. This explains 
undoubtedly the results sometimes obtained by the injection of osmic 
acid in neuralgic nerves and especially in tic douloureux. 

These traumatic causes are especially prolific of the localized forms 
of neuritis. Ofttimes they are never anvthing more than mere excit- 
ing causes. 

The intoxicants are very significant factors in the production of 
neuritis. These and the infections give rise to generalized rather more 
frequently than localized neuritis. In fact, without a determining local 
insult of some sort they may almost be said to never produce a neuritis 
in a single nerve. An infectious process, like an abscess or a tuber- 
culous gland, a cancer or a syphilitic patch, may light up the inflamma- 
tion in a neighboring nerve. Alcohol, lead, arsenic and other metallic 
poisons, carbonic acid, carbon disulphide, ptomaines, nicotine, are all 
to be blamed sometimes for neuritis. 

The infections that have preceded the malady are diphtheria, vari- 
ola, typhoid, tuberculosis, influenza, scarlet fever, etc. I have seen 
syphilitic peripheral neuritis of the multiple type, though many doubt 
its existence and attribute it to the use of mercury. Syphilitic neuritis 
of the spinal and cranial nerve-roots is by no means a great rarity. 
Puerperal neuritis is infectious in origin. Leprous neuritis and the 
endemic forms known as beri-beri, akatama, etc., are to be mentioned 
here. 

In many cachectic and constitutional states, like rheumatism, gout, 
diabetes, leukemia, arteriosclerosis, malnutrition and autointoxication 
undoubtedly are the immediate, noxious factors. Arteritis obliterans 
acts largely in the same way, but more locally. 

It is hardly necessary, after what I have said in regard to the 
infections and their importance both as predisposing and exciting causes 
of neuritis, to mention suppurative processes, nearby or remote from 
the nerve. 

Pathology and Pathogenesis. — The whole subject of the pathol- 
ogy of neuritis has been, up to the present time, in a state of chaos. 



THE NON-NEURONIC DISEASES 583 

This was the natural result of the clinical study of these diseases pre- 
ceding the pathological. It must be frankly granted that clinically all 
forms of nerve inflammation and degeneration are practically about 
the same. The two conditions are not only almost always found to- 
gether, but symptomatically they cannot be well distinguished apart. 
When, however, we leave the clinical side of the question and take up 
the pathological, the distinctions are so sharp and so clean-cut that I 
believe much of the confusion can be banished by attempting a positive 
classification of the disease on a purely pathological basis. 

Neuronic and non-neuronic processes underlie the pathology of 
neuritis. The former are degenerative, the latter are inflammatory. 
In some conditions the former may appear alone. It is then a primary 
degeneration and has been unfortunately and erroneously called paren- 
chymatous or degenerative neuritis. As I have shown, it is not a neu- 
ritis at all and should be banished entirely from consideration under this 
head. It is a rare condition and is merely another manifestation of a 
much more extensive condition. It may be seen in locomotor ataxia. 

The much more common form of neuritic degeneration is the 
secondary. A consideration of this is strictly in place here. It is a local 
trouble, is due to extra-neuronic factors, and is always a companion 
of the inflammatory process, though it may sometimes precede, some- 
times follow the latter. 

These two, inflammation and secondary degeneration, go hand in 
hand ; sometimes one, sometimes the other leading. At times the de- 
generation is so slight or the cause of it is so evanscent that the neu- 
rones recover before the interstitial inflammatory phenomena have got- 
ten a fair start. Under such circumstances recovery takes place and 
the disease has all the appearance of having been a temporary form 
of primary degeneration. Such are some of the degenerative poly- 
neuritides, some of the types of Landry's paralysis, some of the severe 
infective troubles that quickly end in death or recovery before either 
degeneration or inflammation has gotten sufficient of a start to produce 
gross, discoverable changes. Doubtless the character of the infection 
and the neuropathic state of the patient determine to a large extent 
the predominence of the degenerative or inflammatory process in this 
twin-like pathological development. In many cases the inflammatory 
process is so violent, the disease is most emphatically a neuritis with 
all the symptoms of an inflammation, the degeneratinn coming along as 
a later and slower process. 

Thus there are not many types of neuritis as authors declare. 
There is only one neuritis in which there is a variable, double pro 
going on. It is simply confusing to talk about perineuritis, interstitial 
neuritis, parenchymatous neuritis, periaxile segmentary neuritis, dis- 
seminated nodal neuritis. One might as well talk about motor neuritis, 
sensory neuritis, neuritis with fever, neuritis without fever, cranial 
neuritis and podalic neuritis. Medicine is too full of such artificial and 
useless refinements of classification. As I have urged before, it is the 
aim and goal of science to combine and generalize a multiplicity of facts, 
not to break what is already plainly combined, into a multiplicity of 
fragments. Primary degeneration being banished entirely from the 



' 



5^4 



THE NON-NEURONIC DISEASES 



neuritides, all of the other forms are but phases of the one combined 
inflammatory degenerative pathological process which for want of a 
better name we call neuritis. 

The inflammatory side of the neuritic picture does not require any 
lengthy description. There is hyperemia, proliferation of the blood- 
vessels, extravasation of blood, leucocytosis, swelling, cedema and all 
the usual signs of an inflammation anywhere. The swelling does not 

FIGURE 132. 




t t 



— Degeneration and regeneration of nerve-fibres, a, nerve-fibre, fifty hours after 
operation, m y, medullary sheath breaking up into myelin drops, p, granular proto- 
plasm replacing myelin, n, nucleus, g, primitive sheath, b, nerve-fibre after four 
days, cy, axis cylinder partly broken up and enclosed in portions of myelin, c, a more 
advanced stage in which the medullary sheath has almost disappeared. Numerous 
nuclei, n" are seen, d, commencing.regeneration ; several fibres (t\ t") have sprouted 
from the somewhat bulbous cut end (6) of the nerve, a, an ajris cylinder which has 
not yet acquired its medullary Bheath. s, s'. primitive sheath Qf the original fibre. 
I'Ranvier.) 

appear uniformly along the whole course, or even a long extent, of the 
nerve. It appears more prominently in foci or spots. These are prob- 
ably the explanation of the tender points of Valleix seen in many cases 
of so-called neuralgia. Sometimes in these spots an exudate appears 
in abundance and later on a proliferation of the connective tissue, af- 
fording ground for the name disseminated nodal neuritis. 

As neurologists we are more interested in the degenerative side of 
this neuritic process than we are in the inflammatory. This is always 
of the secondary or Wallerian type of degeneration. It means that the 
nerve fibrils have been more or less severed from their nutrient centers. 



THE XOX-XEUROXIC DISEASES 585 

I have described this process elsewhere. The medullary white substance 
of Schwann on the distal side of the lesion, breaks down into fat 
globules, is reabsorbed and leaves nothing but the axis-cylinder and 
the neurilemma. The neuclei of the latter proliferate. The axis-cylin- 
der swells up, liquifies and breaks down into fragments. Gradually 
these are absorbed so that nothing is left but the neurilemma in the 
shape of a hollow tube filled with liquid matter and nuclei. Ranvier 
regards the nuclear proliferation as the primary part of the process, and 
the breaking up of the myelin sheath as the result of it. Alterations 
take place simultaneously in the epineurium and perineurium, so that 
the nerve becomes smaller and harder, in fact sclerosed. The termina- 
tions of the nerve in the muscles and the end-plates ail participate in 
the degeneration. Forty-eight hours witnesses these changes and at 
the end of a couple of weeks they are complete. The cut end of the 
nerve shows the absence of the fibres and the hyperplasia of the con- 
nective tissue. 

The muscles innervated by the damaged nerve also degenerate. 
The fibres diminish, lose their striations, become granular or waxy. 
There is proliferation of the sarcolemma and the internal perimysium. 
Finally the whole muscle atrophies and becomes fibrous or cirrhotic. 

The nerve on the proximal side of the point of severance or lesion 
undergoes the change known as the reaction a distance. This is a de- 
generation of a slower and less complete type, probably due to the ab- 
sence of normal stimuli. 

The course of the degeneration follows the well-known Wallerian 
laws. Thus if the posterior spinal nerve root be cut between the 
ganglion and the cord, the degeneration occurs in the end attached to 
the cord and passes even into the cord. The end attached to the 
ganglion remains intact. Motor nerves and the anterior nerve roots, 
when cut, degenerate downward in their distal parts. The spinal at- 
tachment does not degenerate. 

The regeneration of a nerve is a most interesting and important 
process. It can only take place when the degeneration has not gone 
on to completion. In some compression neuritis degeneration of a 
partial character and regeneration undoubtedly take place with great 
rapidity, so that profound symptoms are often seen to quickly appear 
and disappear. In a severed nerve that has been sutured the process 
of neurolization takes place, though it is denied by some. It consists of 
a growing forward of the axis cylinder from the central stump into the 

red end. If the nerve fibrillar are given a bridge of decalcified 
osseous matter or a fine bundle of catgnt over the lesion, they will ad- 
vance all the more rapidly and completely. In this they resemble the 
advancing branches of a growing vine. Months and years arc some- 
times required for the regenerative proc 

Symptoms. — When a nerve is damaged there will be motor, 
sensory, trophic, reflex, electrical, vasomotor and secretory disturbances. 
The character. of these and the degree of their severity will vary in 
accordance with the complete or partial character of the damage done. 
There are early signs of irritation, followed by ti less 

complete paralysis. It cannot be too strongly impressed upon the mem- 



586 



THE NON-NEURONIC DISEASES 



ory that nerve lesions show signs of irritation and paralysis, in all 
functions, in the areas particularly innervated by the nerve involved. 

The motor symptoms are spasms and twite kings in particular mus- 
cles or muscle groups, followed by a flaccid paralysis more or less pro- 
found. It is soon followed by the loss of reflex response, the electrical 
reaction, of degeneration and atrophy. . 

The early symptoms in the sensory sphere are parcesthesice of vari- 
ous sorts. There are numbness, tingling, pins-and-needles sensation, 
sense of heat, ants crawling on the skin or formication. Soon pains 
occur both along the course of the nerve, especially upon pressure, and 
in its peripheral distribution. On account of the pressure on the nervi 
nervorum the pains seem to shoot here and there along the course of 
the nerve. The skin becomes hy paresthetic. Late in the disease it be- 
comes hyp aesthetic, rarely anaesthetic. A curious and almost path- 
ognomic feature about the sensations is that they are in spots and that 
hypaesthetic areas will be intermingled with hypersesthetic areas. The 
sensory and motor disturbances attack corresponding parts, showing 
thus the limitation of the disease process to particular nerves. In neu- 
ralgias, so-called, often the neuritic character of the disease is shown 
by the local tenderness, the painful swellings which can be felt by 
palpation and which are probably identical with Valleix's tender points, 
and by the special tenderness of the nerve where it passes over bony 
prominences. 

The trophic disorders of neuritis include a glistening of the skin, 
herpetiform eruptions, pemphigus, gangrene, formation of slow healing 
sores, changes in the bone, subcutaneous tissues, hair, nails, etc. 

The vasomotor and secretory troubles are local hyperemia or 
cyanosis, with corresponding change of temperature, oedema, hypert- 
drosis. 

Fever and chills sometimes occur early. 

Diagnosis. — The chief signs of neuritis, whether it be prominently 
degenerative or inflammatory, is the gradual break in all functions in 
the parts supplied by the particular nerves. Especially significant, how- 
ever, are the early irritative signs, such as spasms, tonic contractions, 
sharp pains and paresthesia, followed by flaccid, atropine paralysis, 
with loss of reflexes and reaction of degeneration. One can hardly 
make an error of diagnosis if he is careful to get all of these symptoms 
and view the picture formed by them in toto. It points distinctly to a 
lesion of a mixed nerve. 

The differential diagnosis of neuritis from neuralgia and from con- 
ditions in which it occurs as a side issue, will be taken up more con- 
veniently in the discussion of these other diseases. 

Prognosis. — Except in the mildest cases of compression, when 
recovery may take place in a few days or weeks, the course of neuritis 
is usually a prolonged one, six months or a year at least being its aver- 
age duration. The prognosis depends upon many factors. When the 
disease occurs in an alcoholic or a victim of lead intoxication, infection 
or other general cachexia, it is apt to be severe and last long, though 
the exciting cause may seem to have been insignificant. The virulence 
and character of the toxin in the toxico-infectious cases determines the 



THE NON-NEURONIC DISEASES 587 

prognosis. Some toxins seem to light up a violent inflammatory condi- 
tion, which soon subsides upon the removal of the cause ; other toxins 
provoke a more gradual degenerative state with a mild degree of asso- 
ciated inflammation, which becomes chronic and even leaves a perma- 
nent defect. When the nerve is completely severed the restitution does 
not occur for months and sometimes not at all unless the stumps are 
sutured together. 

Cases in which it used to be thought that the neuritis ascended into 
the cord are very doubtful. Most of them have been toxic cases and 
the degeneration has been rather of the primary type with the nutritive 
functions of the central cells damaged by the general toxaemia. 

The prognosis can usually be based upon the electrical phenomena. 
If the reaction of degeneration is slight, recovery may be expected early. 
If the reaction of degeneration is complete, the course of the disease 
will undoubtedly be prolonged, and perhaps there will be some perma- 
nent defect left in the function of the nerve. Death does not occur from 
neuritis, unless the nerves involving the heart and respiration are af- 
fected. Permanent annoying paresthesias, pareses, trophic manifesta- 
tions need not cause surprise, though they cannot be said to be common. 
Rheumatic and acute infectious cases offer, as a rule, the most hopeful 
outlook. 

Treatment. — The cause, if it can be discovered, must be removed 
promptly and thoroughly before any treatment is instituted. In the 
majority of the cases practically this, and putting the limb at rest, are 
all that will be necessary. In removing the cause both medicinal and 
surgical resources may have to be called upon. Diatheses, such as 
rheumatism, tuberculosis, malaria, syphilis, must be combated in the 
usual way. Abscesses must be drained ; cancerous foci must be re- 
moved ; diseased glands must be cut away. It hardly needs to be said 
that alcohol, lead, arsenic and other poisons must be stopped and rapid- 
ly eliminated from the system. Luxations and subluxations, fractures, 
exostoses, cicatrices, compressing tumors mav all have to be removed 
before anything can be done with the inflamed nerve. 

If the nerve has been severed through an open wound, the wound 
sh< -uld be enlarged, if necessary, and the ends of the nerve approximated 
promptly by sutures. Primary suturing has given some excellent re- 
sults and prevented paralyses and other troubles. For the details of 
nerve suturing works upon surgery should be consulted. 

The cause having been attacked as completely as ]>■ ssiWe, an anti- 
phlogistic treatment may be in order. ( )ften. however, simple rest and 
quiet is all that is necessary. In the violently inflamed cases cathartics, 
aconite, general diaphoresis with wet packs, and hot baths may all be 
thought of. Locally leeches, hot sand bath, hot compresses and later on 
inunctions of gray ointment, the use of vesicants and light touches with 
the Paquelin cautery are valuable. In the degenerative cases the anti- 
phlogistic methods need not be so vigorous. Re>t and antispecific medi- 
cation is about all they require. 

There is probably no class of troubles more than the neuritides in 
which the doctrine of laissez-faire produce- its happiest results. I am 
convinced that had electricity never been introduced into therapeutics, 









588 



THE NON-NEUROXIC DISEASES 



more cases of neuritis would have gotten well. It is a curious fact how 
electrical treatment is at once thought of the moment the diagnosis 
of neuritis is made. It would seem that some have the idea that elec- 
tricity is a sort of a beneficent angel for all diseased nerves. Only let 
it once get at the nerve and recovery will be sure to take place. As an 
actual fact electricity has been the bane of diseased nerves, for in being- 
used too early and in all cases alike, it has simply rasped and irritated 
them and increased the trouble tenfold. I have frequently seen a case 
of neuritis slowly but surely recovering suddenly sent into a severe 
relapse because the attendant labored under the delusion that a diseased 
nerve was the golden opportunity for him to flourish forth his electrical 
paraphernalia. The more my observation enlarges the more I am 
convinced that few and far between are the occasions when the electrical 
treatment of neuritis is called for. If it can be absolutely determined 
that the disease is prominently of the degenerative type, and that there 
is no inflammatory action going on — a condition which it is almost im- 
possible to determine — electrical treatment with galvanism may and 
does prove of much avail. Such a condition does occur very late in the 
violently inflamed cases, and earlier in the mildly inflamed. Hence it is 
absolutely imperative that electrical treatment should be postponed until 
all signs of inflammation are gone. In this stage of the disease elec- 
tricity and massage are of invaluable service. The kind of electricity to 
be employed will depend upon the site of its application and the degree 
of degenerative reaction present. Galvanism is to be used upon the 
nerves, faradism upon the muscles. If there is much degeneration pres- 
ent, the reaction of it may be so pronounced that neither the galvanic 
nor faradic current will awaken a response. This is, however, rarely 
the case. More frequently a partial reaction is present. Under such 
circumstances the faradic response may be wanting and only the gal- 
vanic be present. In using the galvanic current the anode may be 
placed upon the plexus or sternum, and the cathode upon the points 
indicated in Erb's diagrams in the chapter on electrotherapeutics. A 
stabile current is to be used and its strength should average about five,, 
ten or fifteen milliamperes. Labile galvanic stimulation of the muscles 
may be added to the treatment. Faradic stimulation is to be used as 
soon as the faradic irritability returns. It is never to be used if there is 
the slightest sign of inflammation present. It is positively dangerous in 
the early stages of the disease. Later on it is more beneficial. Evert 
static electrization is good in the later stages. 

Massage must not be employed too early either. As a restorative 
massage is second only to electricity. It is not well to rub directly over 
the nerve, but along side of it. The manipulations must be gentle and 
towards the body, and the seances should be daily. 

Invaluable as electricity and massage are in the treatment of the 
degenerative results of neuritis, I must repeat the caution not to use 
either in the early stage of acute inflammation. Atrophy, contractures 
and shortening can be controlled by them as well as by systematic 
active and passive exercise. 

Recently surgery has been accomplishing some brilliant feats in 
old neuritic cases. A number of operations in the way of secondary 



THE NON-NEURONIC DISEASES 589 

suturing, transplanting and grafting of nerves have been practiced with 
.great success. 

The distal end of a bisected nerve may be united with the prox- 
imal end of another that has been uninjured. The facial and hypo- 
glossal have thus been united. Where there has-been a break in a nerve 
transplantation of nerves from animals has been successfully performed. 
If the break measures more than about four centimetres, the results are 
not so promising. Nerve tumors have been extirpated and the ends of 
the stumps thus approximated. Nerves have been freed from tumors, 
cicatrices, callus and exostoses, even after sixteen years' standing, and 
restoration of movement and sensation obtained. Ofttimes splints and 
bandages have to be worn for some time after these operations. Elec- 
trical treatment is also later on called for and should be continued for a 
year. 

MULTIPLE NEURITIS. 

Paralysis and sensory disturbance was observed long ago to fol- 
low the ingestion of alcohol, certain febrile exanthemata, constitutional 
cachexia and poisons of various sorts. Such paralyses were spoken of 
as alcoholic, lead, febrile, diabetic palsy, etc. Most excellent descrip- 
tions were given of it by Jackson, Huss, Lancereaux, Duchenne and 
others. Most of the theories propounded to explain it attributed it to 
disease of the brain or spinal cord. In 1864 Dumenil made the first 
careful post-mortem examination of a case dead from alcoholic paralysis 
and announced that the peripheral nerves were diseased while the cord 
and brain seemed to be perfectly normal. Though at first neglected, 
Dumenil's observation soon began to be confirmed by the observations 
of others, notably Eichhorst, Joffroy and Leyden. The last observer 
finally established the disease, in 1880, as a distinct entity. Since the 
work of Leyden, our knowledge of the malady has been steadily ad- 
vanced by the investigations of Eisenlohr, Striimpell, Ross, Buzzard, 
Hun, Mills, Cole and many others. That there is such a disease as a 
pure, uncomplicated polyneuritis is undeniable ; that it is rare is being 
more and more recognized. As an associated trouble with general con- 
stitutional intoxication and disease of the central nervous system it is 
very frequent. Many problems still await a solution in regard to its 
pathogenesis, its extent and distribution, its complications and accidents 
and associated troubles, the essential nature of its disease-process, the 
differential diagnosis and pathology of its various forms, its course and 
prognosis and its proper management. 

Etiology. — The causes of multiple neuritis are numerous. Under 
the head of pathology will be discussed the various types of the disease 
with mention of the etiological factors that play the principal role in 
each type. In the vast majority of cases intoxication and infection are 
the causes. This is so overwhelmingly the case that it is beginning to 
be believed that all other causes than intoxication and infection serve 
merely as excitants and not as essential etiological factors. Alcohol 
is the supreme toxic cause, especially when taken steadily, though mod- 
erately, for a long period of time. It matters but little whether it is 
imbibed in the form of whisky, beer or wine, so long as it sets up a 






59o 



THE NON-NEURONIC DISEASES 



state of chronic alcoholism. After alcohol we find that the disease is 
caused by ether intoxication, bisulphide of carbon, carbon dioxide, 
naphtha, lead, arsenic, coffee, mercury, anilin, ptomaine and leucomaine 
poisoning. It has been attributed to sulphonal and other drugs and 
medicinal preparations. Among the infectious antecedents we note 
leprosy, typhoid fever, variola, scarlatina, influenza, diphtheria, erysipe- 
las, purulent pleuritis, acute articular rheumatism, mumps, gonorrhoea 
and dysentery. To these must be added tuberculosis, syphilis, malaria, 
diabetes mellitus, severe anaemia, carcinoma and marasmus from any 
cause. Septicaemia and puerperal fever have preceded its outbreak. 
It has been charged to alimentary autointoxication, constipation and 
putrid bronchitis, icterus and hepatic cirrhosis. 

Akatama, kakke and beriberi are endemic forms of the disease 
doubtless due to an infection. 

The senile form of the disease has been attributed by Oppenheim, 
Joffroy, Gombault, Schlesinger and others to arterio-sclerosis and 
arteritis obliterans. 

Exposure to cold, overexertion, mental and nervous strain are 
provocative only in the presence of other conditions, such as those 
mentioned above, and hence are to be regarded more in the light of 
mere exciting or initiatory causes. 

The middle period of life, when the above causes are most in 
evidence, is the time when multiple neuritis is most frequently met with. 
In children the diphtheritic form is the most common as well as those 
forms that are due to scarlatina and other infantile infections. In old 
age the cachectic forms of the disease predominate. Women are the 
victims of the alcoholic type far oftener than men. Other etiological 
factors of the disease depend upon the etiology of the underlying con- 
stitutional intoxication and infection. 

Pathology and Pathogenesis. — The characteristic pathological 
finding of multiple neuritis is a parenchymatous degeneration of the 
peripheral nerve ends. By the older writers this was supposed to be a 
secondary result of an interstitial inflammation of the nerve trunk or of 
a primary parenchymatous inflammation. Hence the name neuritis, 
and its division into interstitial and parenchymatous neuritis. No 
pathologist of repute nowadays speaks of the latter as an inflammation. 
As a result of the direct action of the alcohol and ether poisons upon 
the nerve fibre or its cell, a degenerative process occurs. Therefore 
we speak at present of two great classes of neuritides, namely, those of 
inflammatory (interstitial or periaxial) and those of degenerative 
(parenchymatous, axial) origin. They are the same disease, however. 
As I have explained under the head of neuritis, this is a degenerative 
trouble, not of the purely primary type, but of the combined degenera- 
tive and inflammatory type. Both processes are dependent upon the 
same cause and are mutually to a certain extent dependent upon each 
other. Sometimes one, sometimes the other is the more prominent 
feature of the disease, but both go together. Under this conception we 
find that polyneuritis can be conveniently subdivided into three general 
classes, all of which differ slightly from one another in regard to 
etiology, symptomatology, pathology, prognosis and treatment. 



THE NON-NEURONIC DISEASES 59 1 

In the first class, perhaps the most typical, certainly the largest 
class, we include the neuritides of the degenerative type, whether the 
primary cause be toxic (alcohol, arsenic, mercury, etc.) or infections 
(typhoid, variola, puerperal fever, tuberculosis, syphilis, etc.) or 
cachectic (diabetes, carcinoma, marasmus). Some of these are primary 
degenerations and, as 1 have noted elsewhere, are but side issues, as it 
were, of other diseases. They are not special any more than tubercu- 
lous glands would be special diseases apart from general tuberculosis. 

In the second class may be conveniently grouped the neuritides, 
neuritis of the inflammatory type, in which the parenchymatous degen- 
eration is entirely secondary. These cases include the endemic, infec- 
tious types such as leprosy, beriberi and certain forms of unknown 
origin. 

In the third class both inflammation and degeneration play a role 
in their origin. They are the neuritis of diphtheria and some primary 
forms of unknown origin. The second and third class are the true 
types of neuritis. 

In all forms of multiple neuritis the inflammatory signs are never 
as prominent as are the degenerative. There may be in some of them 
redness and swelling of the nerve trunk and hyperemia of the sheath. 
Even minute hemorrhagic extravasations with all the usual manifesta- 
tions of a severe local inflammation may be seen here and there along 
the course of the nerve. This is not common, however. More fre- 
quently there are no discoverable interstitial changes ; only more or less 
atrophy of the individual nerve-fibres. The myelin substance is broken 
into clumps; the contour of the fibre is irregular in outline; and the 
fibres are reduced in size and diminished in number. Among this mass 
of wasted and diminished fibres some are seen to be regenerating, while 
others retain their normal, healthy appearance. The disease process 
in many cases seems to grow less, both in severity and extent, as we 
ascend the nerve trunk. The point of transition from diseased to 
healthy nerve tissue varies in different cases and in different nerves 
even in the same case. 

In some of the cases the lesion is limited to the peripheral nerve- 
fibres. This is especially true of the diphtheritic cases, wherein the 
poison acts directly upon the nerves in the immediate neighborhood of 
the infected focus. Nevertheless, in the diphtheritic cases and much 
more so in the other toxic and infectious cases, foci of disease are found 
in the spinal nerve roots, the spinal cord and its membranes. In alco- 
holic, lead and other cases, the myelitic and encephalic evidences of dis- 
ease are being discovered post-mortem more and more frequently. 
These partake of the nature of poliomyelitic and encephalitic processes 
with atrophy of the cells. On account of this the view is growing that 
in these cases the toxin affects the entire nervous system, of which 
the polyneuritis is> but one of many local expressions. In this way its 
great variety of symptoms is explained. Some attribute the neuritis 
even to the functional damage done to the cells in the cord by the poison. 
Cole and others among the most recent investigators frankly affirm that 
multiple neuritis, especially of the alcoholic type, is a widespread affec- 
tion of the nervous system ; that the central changes are not attributable 









592 THE NON-NEURONIC DISEASES 

to the peripheral trouble ; that the lesion of the peripheral 
neurones is only one of many manifestations of the disease 
and is accompanied by lesions identical in nature, affecting many 
groups of neurones situated entirely within the central nervous system ; 
that though in some cases' the peripheral neurones are mainly affected, 
in others the morbid process implicates chiefly the central neurones, 
two groups of cases which do not appear, however, to be sharply divided. 
The same is true, though not to the same marked degree, in regard to 
the other forms of polyneuritis, especially those due to lead and arsenic 
and in which mild delirium occurs with febrile phenomena. As the 
bacterial products and not the bacteria themselves are credited with the 
production of the disease, it is not surprising that the infectious cases, 
like the toxic, should show the same general characteristics in regard 
to the entire nervous apparatus. 

Symptomatology. — Charcot used to contend that peripheral neu- 
ritis is not a distinct disease, but a substratum underlying the symptoms 
of several very different affections. His contention was supported by 
the dissimilarity in the clinical pictures presented by the different forms 
of multiple neuritis. Even to-day we are obliged to discuss the symp- 
tomatology of alcoholic, lead, arsenic, diphtheritic paralysis, etc., under 
their own respective heads. Unlike as they are in many respects, these 
various forms of multiple neuritis present a sufficiently constant and 
uniform set of symptoms to base a clinical description upon. As the 
alcoholic type of the disease is the most common and uniform, it will 
be described first as a sort of symptomatic model. 

I. Toxic Forms; (a) Alcoholic Type. — The first symptom 
noticed by the patient is a paresthesia in the feet and hands. It comes 
on more or less suddenly and consists of numbness, "pins-and-needles"' 
sensation and a feeling of pricking. There may be actual pain in the 
limbs, sharp and shooting or dull and rheumatoid in character. These 
early sensations may occur in the course of chronic alcoholism or after 
an attack of delirium tremens. Occasionally the temperature may be ele- 
vated, but as a rule there are no febrile manifestations. The paresthe- 
sia is bilateral in distribution. It attacks all four limbs about in the 
same way and gradually ascends toward the hips and shoulders. The 
pains are irritating, may be sharp or dull, may come and go in the 
course of particular nerves, and gradually lessen in severity as the 
disease advances. A feeling of weakness appears in the limbs in a few 
days and the muscles and tendons begin to feel like stiff parchment to 
the patient, or as if they were tense and just a little too short. Between 
the numbness, weakness and slight rigidity, the patient cannot coordi- 
nate his movements and so finds difficulty in walking and using the 
hands. In a little while the weakness passes into an actual paralysis. 
This seems to involve the extensor more than the flexor muscles, caus- 
ing wrist-drop and ankle-drop. All the nerves of the extremities may- 
be involved, but the musculo-spiral and the anterior tibial seem to be 
especially affected. The muscles of the trunk and head as a rule escape 
and the mind is affected in a particular way only in certain cases. The 
reflexes are lost, both deep and superficial. The muscles are noticeably 
wasted and if tested electrically exhibit more or less completely the 



THE NON-NFURONIC DISEASES 593 

reaction of degeneration. There is some anccsthesia, distributed gener- 
ally or in spots over the limbs. Hyperalgesia is often a valuable symp- 
tom and the local tenderness in the muscles and nerve trunks is so 
characteristic a sign that it helps to differentiate the disease from other 
affections with similar disturbances of sensation and motion. Hyper- 
esthesia may be discovered in areas of the skin alongside of areas of 
hypaesthesia. As a result of the sensory disturbances ataxia may be 
present. Hyperidrosis, oedema, szvelling in and about the joints and 
even certain skin eruptions and ulcers may be expected among the later 
vasomotor, secretory and trophic manifestations. The rectal and vesical 
functions as a rule are unaffected. Such in outline is the clinical pic- 
ture of a typical multiple neuritis. Such a pure type, however, is rare 
and it is therefore necessary to consider some of the symptoms a little 
more in detail. 

The more prominent of the sensory symptoms, being subjective in 
character, are less valuable as symptoms than some other signs on that 
account. They are indicative only of the disease when studied as a 
part of the clinical picture in toto. If taken by themselves they may be 
mistaken for hysterical and other psychoneurotic manifestations. 
Though the sensory phenomena are rarely absent, they assume the 
most varied and bizarre characteristics. For instance, in the soles of 
the feet all qualities of sensation may be decreased or lost ; or there 
may be anaesthesia with hyperalgesia or hyperesthesia with analgesia. 
A very common combination which I have seen often is anaesthesia with 
hyperesthesia in adjoining areas. The touch and muscular senses may 
be diminished, while the pain sense is highly exaggerated, or vice versa. 
Instead of being diminished the sensations may only be delayed. In 
the trunk a rare girdle sensation is sometimes found, but it belongs to 
the other symptoms of central disease usually accompanying alcoholic 
neuritis. It is to be noted carefully that these sensory manifestations 
are symmetrical in distribution, that they are more extensive than the 
corresponding paralysis, that they are partly subjective and objective 
in character and that they exhibit the variability and irregularity that 
one would expect from a variable lesion involving a large number of 
separate and unrelated peripheral nerve fibres. Such an incongruous set 
of phenomena could only be imitated by a pure psychosis, but a psycho- 
sis can easily be distinguished from a polyneuritis by other symptoms. 

Much more striking than the sensory symptoms is the motor 
paralysis. In some forms of multiple neuritis this is almost the only 
symptom. It is of course of the flaccid, degenerative type of paralysis, 
since the lesion involves the lower or peripheral motor neurones. It is 
always accompanied by distinct muscular atrophy and alterations in the 
electrical reactions. It is usually more profound in the legs than in the 
arms, though great variations are possible as to the areas of its distribu- 
tion. In some respects it resembles marvdously the paralysis of an- 
terior acute poliomyelitis, for it may involve one leg or certain muscles 
only in that leg, or only certain muscles in all four limbs or even all the 
muscles of all the limbs. Curiously where a nerve innervates more than 
one muscle, it sometimes happens that one muscle will be paralyzed 
while the others escape. The nerves may show the electrical reactions 



594 



THE XOX-XEUROXJC DISEASES 



of degeneration and yet their corresponding muscles not be paralyzed. 
The peculiar character of this paralysis has even led some to think that 
the disease is primarily a toxic injury of the cells of the anterior horns 
of the cord with a mere secondary degeneration in the peripheral 
axones. Though this is not entirely acceptable, it is undoubtedly true 
that in some cases, at least, the pathological process and its resulting 
paralysis is partly poliomyelitic as well as neuritic. 

In some cases ataxia rather than paralysis is the chief motor mani- 
festation. It is rare, however, and is the symptomatic basis of the 
peripheral pseudo-tabes of Dejerine. It is often associated with anaes- 
thesia, and implicates the legs much more often than the arms. Of 
course, it changes the gait and active movements and may lead to an 
erroneous diagnosis of locomotor ataxia. Involuntary muscular twitch- 
ings sometimes accompany it. 

The atrophy and tenderness of the muscles are two characteristic 
symptoms of this disease. They are most always present and when 
found together in the same patient are pathognomonic. The wasting of 
the limbs is marked and rapid. It is not as severe and rapid perhaps, 
nor does it pick out individual muscles so strikingly, as does the atrophy 
of infantile palsy. It may for a time be obscured by oedema or fatty 
deposits. The muscles feel soft and flabby, are cold and somewhat pale 
in color. Pressure and passive movement oiten cause such intense pain 
that it is impossible to make a complete examination. 

Abolition of the deep reflexes is the characteristic of polyneuritis. 
Usually this is complete and early in appearing. Sometimes, however, 
it is for a brief time preceded by an exaggeration. Occasionally it is 
incomplete and capable of being partially elicited by reinforcement. The 
paralysis in such cases is a partial one. 

The cranial nerves are frequently involved, though their implica- 
tion is in no way pathognomonic. The same may be said of the brain. 
And yet it is not to be wondered at in view of the frequency with which 
disturbances of the brain and cranial nerves are met with that many 
are beginning to look upon them as essential manifestations of the dis- 
ease and not as mere complications and accidents. In other words, the 
view is spreading that the polyneuritis is but one manifestation of a 
much more extensive disease process, namely, a toxic degeneration of 
the entire nervous system (Buzzard, Cole and others). 

Among the cranial nerves the third is most often affected ; next the 
sixth. Reflex pupillary rigidity is rare, but nystagmus, diplopia and 
ptosis may all be looked for. Very seldom is the optic nerve involved, 
though optic neuritis and even partial optic atrophy have been observed 
several times. There may be a central scotoma, especially for colors. 
Among the other cranial nerves that may be involved are the facial, the 
vagus and phrenic and the nerves of mastication and deglutition. 
Strumpell saw the auditory nerve involved. A polyneuritis limited to 
the cranial nerves would be a curiosity, and yet such has been referred 
to by Hosslin and. Mannaberg. 

The mental symptoms of alcoholic neuritis are deserving of special 
consideration. They consist of failure of memory, confusion and loss 
of the proper conceptions of time and space. Korsakoff was the first 



THE NON -NEURONIC DISEASES 595 

to name and systematize this polyneuritic psychosis, though others had 
observed and described it before him. Amnesia, disorientation, pseudo- 
reminiscence and confabulation are its chief characteristics. Events of 
the past are spoken of as about to occur in the future and vice versa. 
Hallucinations and mild delusions are sometimes present. They are 
easily repressed. Occasionally they are determined by the sensory 
symptoms. One of my cases spoke of having just been out in the gar- 
den picking flowers and getting covered with burrs, when, as a matter 
of fact, it was a cold, midwinter day and she had not been out of bed for 
ten days. By many this confusional type of psychosis is regarded 
merely as an alcoholic complication of the polyneuritis. Others attribute 
it to a mild toxic encephalitis, which, like the peripheral neuritis, is one 
of the outward expressions of the underlying chronic toxaemia or alco- 
holism. The hypothesis has even been set up (Turner) that it is the 
result of the isolation of the patient's mind by the shutting off of his 
normal afferent impulses through the widespread neuritis. If alcoholic 
polyneuritis is a distinct disease in itself, then these mental manifesta- 
tions are of the nature of pure complications or accidents. If, however, 
the real disease is an alcoholic degeneration of the entire nervous sys- 
tem, with peripheral neuritis as one of its outward expressions, the 
central symptoms will then have to be regarded in the light of another 
set of outward manifestations. 

Alcoholic polyneuritis in the majority of instances runs an acute 
of subacute course and its prognosis is in the main favorable. It ap- 
pears rather abruptly, rises to its climax in a few weeks or months, 
remains stationary for about the same time and then gradually recedes. 
There are violent cases that run a rapid course and terminate in death 
in a few days. In such cases the cranial nerves, especially the vagus 
and phrenic, are likely to be involved. The general condition of the 
patient, the implication of the cranial nerves, the extent of the paralysis, 
and the degree of muscular atrophy are all factors that influence the 
prognosis. Rarely the disease runs a progressive or even remitteni 
chronic course. Occasionally recovery is complete; more frequently it 
occurs with some more or less permanent defect. This is especially true 
of the cases with mental symptoms. Convalescence is always slow and 
tedious. Irritative symptoms, like pain, disappear first; then the 
anaesthesia gradually clears up or is replaced by paresthesia ; and 
finally after a long time the hyperesthesia diminishes to normal. Some- 
times two years have to elapse before all signs of paralysis have van- 
ished. Relapses are not uncommon. Permanent paralysis in particular 
muscles, and contractures and deformities from overaction of antag- 
onistic muscles, are unfortunately possible. 

(b) Lead Type. — Lead intoxication produces a polyneuritis strik- 
ingly unlike the other forms of the disease in some respects. It was 
this fact that led Charcot to contend that multiple neuritis is not a dis- 
tinct, uniform disease. Motor paralysis confined to a certain area., 
without distinct sensory disturbances, constitutes the predominant fea- 
ture in its clinical exhibition. That the disease, however, is an intoxica- 
tion of the entire nervous system is shown by the brain symptoms and! 
the arthritic pains. The ingestion of lead is the cause of the disease ; 



596 THE NON-NEURON IC DISEASES 

though it has been seen as an inheritance in children whose parents have 
been lead workers. There are many sources from which the lead enters 
the system. Painters, type-setters, pipe-layers and other workers in 
lead ; potters using lead glazes ; weavers handling leaden weights ; 
users of cosmetics containing lead ; washers of bottles employing lead 
shot ; and drinkers of water drawn through lead pipes are all exposed 
to the disease. So extensive is the use of the metal in modern industry 
and so insidious at times is the onset of the paralysis that only a most 
painstaking search will reveal the source of the intoxication. 

In many cases the motor paralysis is the only symptom ; in all 
cases it is the characteristic symptom. When it is preceded or accom- 
panied, as it is usually, by lead colic with its griping pains in the abdo- 
men, by arthralgia with its pains and soreness in and about the joints 
and muscles and especially by encephalopathia saturnina with its mental 
manifestations, the diagnosis cannot be mistaken. The blackish streak 
or blue-black coloration of the gums along the edge of the teeth, the 
anaemia, the cachectic state, the disease of the kidneys and the arterio- 
sclerosis all indicate the wide extent of the intoxication and help to 
confirm the true origin of the palsy. 

As I have said, this palsy is striking and pathognomonic almost, 
for it is never, or rarely, accompanied by sensory phenomena, is limited 
practically to the arms and preferably to certain muscles. It is a 
degenerative paralysis as shown by the loss of reflex action, the marked 
atrophy of the muscles and the electrical reaction of degeneration. It 
involves the peripheral muscles of the limbs symmetrically, showing a 
remarkable selective action. Occasionally certain muscles individually 
are picked out as in infantile palsy. At other times the disease is limited 
to one arm. This is usually determined by the patient's occupation, the 
arm or muscles most employed being the first to succumb. The ex- 
tensors of the hand and fingers are particularly liable to the paralysis, 
resulting in the easily recognized "wrist-drop" and flexion, of the fin- 
gers. If the feet are involved, as rarely they are, the peroneal nerve 
distribution is the one mostly diseased. The tibialis anticus muscle 
usually escapes under such circumstances. There is no uniformity with 
which the muscles of the arms are involved, but in typical cases the 
supinators, especially the supinator longus and the triceps, are spared. 
The extensor carpi ulnaris and the abductor longus pollicis are also un- 
affected as a rule. In other words, the radial nerve and its distribution 
is in the more typical cases the focus of the disease. In other cases the 
smaller muscles of the hand and thumb under the control of the ulnar 
and median nerves are also paralyzed. Still more rarely the interossei 
muscles and the deltoid are paralyzed along with the extensors. In 
Remak's upper-arm type of the disease, which, however, is atypical, the 
biceps brachialis interims and deltoid are implicated. 

Associated with the paralysis there is generally a certain degree of 
fibrillary tremor, swelling a1x>ut the wrist-joint and rarely thickening 
of the metacarpal bones. 

A generalized form of the disease beginning acutely with fever 
and following a saturnine encephalopathy involves all the muscles of 
the arms, legs and trunk. 



THE NON- NEURONIC DISEASES 597 

The cerebral disturbances that often accompany saturnine poly- 
neuritis are numerous and important. They may be general or focal, 
organic in origin or functional. In this way hemiplegia and hemi- 
anaesthesia, temporary or permanent, may he occasionally observed. 
Convulsions, delirium and coma may be preceded by vertigo, tinnitus 
aurium, restlessness and insomnia. There may be distinct hallucina- 
tions of sight and hearing and all the manifestations of acute delirium. 
The cranial nerves may all be affected, optic neuritis and implication 
of the pneumogastric and phrenic being particularly ominous. The 
oculomotorius involvement is shown in mild mydriasis, as I recently 
saw in a very obscure chronic case of general lead intoxication. In 
chronic encephalopathia melancholia with delusions is the more common 
manifestation. The mental power fails or there are exalted delusions 
as there are in dementia paralytica. A degenerative meningoencephal- 
itis is the pathology in these cases. Hemorrhages, local encphalomala- 
cia with arteritis may occur here as in anv form of severe intoxication 
or infection. 

The prognosis of this form of multiple neuritis is favorable in the 
earlier stages of the disease and before grave paralyses have occurred 
or such serious complications as saturnine cachexia, nephritis, optic 
neuritis and other organic destruction of the tissues of the brain and 
cranial nerves. Recovery may be hoped for even after the appearance 
of the reaction of degeneration. Several attacks in succession of the 
paralysis add to the gravity of the outlook. 

(c) Arsenical Type. — Intoxication may result from the use of 
arsenical coloring matters in pigments, wall papers, book covers, etc. 
Attempted suicide with arsenic or Paris green may terminate in a multi- 
ple neuritis. Most of the cases of arsenical paralysis are due, however, 
to the excessive medicinal use of the metal in the form of arsenious 
acid or Fowler's solution. 

Symptomatically arsenical paralysis resembles most strikingly the 
alcoholic type and both forms of the disease differ from the saturnine 
and diphtheritic types in the greater prominence of the sensory mani- 
festations. There seem to be two classes of arsenical palsy. In one 
the muscles are decidedly paralyzed, especially the extensors of the 
hands and feet. In the other the sensibility is especially affected giving 
rise to a condition of ataxia or pseudo-tabes. These symptoms follow 
either acute or chronic poisoning and make their appearance in from 
a few days to a few weeks. 

The paralysis in the arms, flaccid and degenerative in character, 
involves usually the same muscles and causes the same characteristic 
attitude as lead palsy. The same is true in the legs. The deep reflexes 
are diminished or abolished and the usual electrical reaction of defen- 
eration is present. Muscular atrophy occurs very rapidly. 

Unlike lead, arsenic poisoning provokes a greater degree of sensory 
disturbance. The sensitiveness of the nerves and muscles to pressure 
is exceedingly acute. There are initial paresthesia of various sorts on 
the back of the forearms and front of the legs. Severe darting pains are 
complained of. Anaesthesia or hyperesthesia may be general or scat- 
tered about in patches. Sensation in general is almost always decreased, 






59^ THE NON-NEURON IC DISEASES 

especially in the feet, hands and fingers. In these pronounced sensory 
cases there is incoordination of such a character that they closely re- 
semble ordinary tabes. The differentiation between the two diseases is 
made largely upon the presence of a true palsy in the arsenical neuritis. 
Though we speak of a motor and ataxic form of arsenical polyneuritis, 
the motor symptoms are more or less present always in both. In these 
ataxic cases the knee reflexes are practically always absent, pains are 
present, and the sensations are diminished in regard to touch, increased 
in regard to pain. Dana, to whom we owe much of our knowledge of 
this pseudo-tabes, saw optic neuritis in one of his cases. In Seelig- 
miiller's case the patella reflex was not lost. 

Psychic disturbances are present in cases of arsenical polyneuritis, 
though they are not so prominent as in some other forms of intoxication. 
The weakness of the memory, the mental confusion, and the dis- 
orientation bear a resemblance to the mental manifestations of alcoholic 
neuritis. Epilepsy and amaurosis have been recorded. 

Among the trophic symptoms, especially in the prolonged and se- 
vere cases, are to be noted herpetiform eruptions on the skin, true 
herpes zoster, pemphigus, erythematous and bullous outbreaks, glossi- 
ness of the skin, alopecia, falling off of the nails and other indications 
of a profound state of cachexia. 

The initial conjunctivitis and gastric irritation are not unfre- 
quently seen in cases in which medicinal arsenic has been administered 
to the limit of tolerance. In many cases the temperature is slightly 
increased and in nearly all of them the pulse is more or less accelerated. 

Recovery is the rule in this form of polyneuritis, though the con- 
valescence may last for months or years. As the bulbar nerves are 
scarcely ever implicated life is rarely jeopardized. Fatalities usually 
result from respiratory or cardiac failure when they do occur. 

(d) Argentic Type. Argyria. — This is an exceedingly rare 
form of polyneuritis. Gowers has reported a remarkable case in which the 
symptoms corresponded almost identically with those of lead poisoning, 
namely, paralysis in both arms of the long extensor of the fingers and 
of the extensors of the phalanges of the thumb without involvement of 
the extensor of the metacarpal bone of the thumb, atrophy of the 
muscles and reaction of degeneration. The legs were not affected and 
there seem to have been no sensory phenomena. The well-known bronz- 
ing of the skin and blue-black line on the gums were present. The 
source of the silver, in this case as well as in the non-neuritic cases of 
argyria generally, was its prolonged medical administration. As sil- 
ver is not employed now as it used to be in the treatment of such 
chronic diseases as epilepsy and spinal sclerosis, argentic intoxication 
is less frequently heard of. Scarcely any cases of multiple neuritis 
from this cause have been reported. 

(e) Mercurial Type. — It has been asserted that there is a mercu- 
rial multiple neuritis. If so we know very little about it. In most of 
the cases so reported there has been a history of syphilis treated with 
mercury. It is an open question whether the polyneuritis was of 
syphilo-toxic or mercurial origin. Schultze, Buzzard and Oppenheim 
have described syphilitic polyneuritis ; others doubt its existence. There 



THE NON-NEUROXIC DISEASES 599 

is no question but that a polyneuritis in a syphilitic may be made worse 
bv the administration of mercury. I have lately seen this most forcibly 
exemplified and it has been confirmed by Minkowski, Engel and Op- 
penheim. The symptoms of hydrargyria point to lesions of the brain 
and cord rather than of the peripheral nerves. They consist of a 
peculiar tremor not wholly unlike that of paralysis agitans, slight loss 
of muscular power in one limb more than the other, pains in the region 
of the fifth nerve and around the joints, formication in the limbs and 
local analgesia, mental irritability, loss of the power of attention, dis- 
tress, insomnia, hallucinations and even maniacal outbreaks. There 
may even be considerable hemipiegic weakness, aphasia and deafness. 
With all this there is no typical paralysis of neurotic origin though 
these cases are ofttimes of great severity and acquire their mercury 
from gross sources as manufactures, mines and the industrial use of 
the metal. The stomatitis, ulceration of the mucous membrane of the 
mouth, fetor, bone necrosis, gastric and intestinal catarrh and other 
symptoms of profound mercurial intoxication are never accompanied 
by the typical signs of a peripheral multiple neuritis. It seems to me 
therefore that the existence of mercurial polyneuritis may be legiti- 
mately doubted and that the reported cases in which there has been a 
history of syphilis are to be attributed to the specific infection. 

II. Infectious Forms. — The infectious forms of polyneuritis do 
not differ symptomatically from the toxic forms though they are de- 
pendent upon such a multiplicity of infective processes. In the main 
they are all alike, differing from one another, as in the toxic cases, in 
some minor details. As the infection is general the lesions of the 
nervous system are of wide extent with a predominance of parenchy- 
matous degeneration. The symptoms are therefore cerebral, spinal and 
neuritic in origin. In some, as in typhoid and scarlatina, they are 
largely cerebral ; in others, as in variola, dysentery and measles, they 
are apt to be spinal ; in still others, as in diphtheria, acute rheumatism, 
erysipelas and puerperal sepsis, they are mostly neuritic. There are 
no fixed rules in this respect, but as the peripheral neuritis is of a varia- 
ble degree and extent common to all of these infective conditions, I refer 
to them under this head, using one or two of the more striking ones, 
like diphtheria, rheumatism and puerperal sepsis, as more or less illus- 
trative of all of them. 

The universal character and wide extent of the intoxication is 
shown by the multiplicity and variety of the symptoms and especially 
by the uncertainty among pathologists as to whether the peripheral 
neuritic degenerations are due to the primary damage of the central 
cells or to a mere simultaneous degeneration in both central cells and 
peripheral processes. Perhaps the larger number of investigators are 
ready to accept both explanations. None of the more recent patholo- 
gists believe, however, but what the interstitial changes sometimes 
found in these cases, and suggestive of true inflammation of the nerves, 
are but late and secondary results of the degeneration. 

(a) Diphtheritic Type. — In about one-quarter of the eases that 
recover from diphtheria a remarkable form of motor paralysis occurs, 
usually appearing from two to three weeks after the subsidence of the 



600 THE NON-NEURONIC DISEASES 

throat trouble, rising to its maximum in two or three weeks more and 
finally disappearing in from two to three months to a year later. The 
lesions of the nervous system seem to be the result of both a local and 
general infection. For this reason some authorities speak of two forms 
of diphtheritic neuritis, the local and the generalized. A true inflam- 
mation of the nerves near the site of the primary infection is believed 
to characterize the local form, while a general specific toxic degenera- 
tion is thought to represent the latter. This may in part be true, but 
I am inclined to think that in the main the process is a generalized 
intoxication which in some cases affects only the nerves round about 
the original focus of infection where the poison would naturally be the 
most abundant and virulent, but not sufficiently so to involve the more 
distant nervous tissues, and in other cases affects both the local and 
more distant nerves. This is shown in the accidental and experimental 
infection of other parts of the body with diphtheria wherein the local 
nerves are again the ones first to be affected, and in the fact that in 
nearly all the cases of generalized and distant neuritis there is or has 
been more or less local neuritis near the primary disease. 

Motor paralysis, flaccid and degenerative, is the predominant 
symptom of this type of polyneuritis. All the usual characteristics of 
disease of the lower -motor neurone, such as loss of reflex action, mus- 
cular atrophy and the electrical reaction of degeneration accompany this 
paralysis. Sensory manifestations are insignificant or entirely absent. 
They are always more or less present when the paralysis is severe, and 
consist of paraesthesiae, such as numbness, tingling, formication or 
anaesthesia, sometimes hyperesthesia or, what is more common, hypaes- 
thesia. All forms of sensation may be altered so that incoordination 
obtains. Aubertin doubts, however, the occurrence of true ataxia. 
Rarely the bladder and rectum are affected and there is a remarkable 
absence of vasomotor, secretory and trophic symptoms. Albuminuria 
is common and in fatal cases almost constant. 

It is to the distribution of the motor paralysis that diphtheritic 
polyneuritis owes its distinction. In the larger number of cases it is 
more or less confined to the muscles of the soft palate. By reason of 
this fluids regurgitate through the nose and the speech is embarrassed 
with a nasal twang. Deglutition is therefore difficult and gargling is 
quite impossible. Puffing of the cheeks and the blowing out of a 
candle can only be accomplished when the nares are compressed. Upon 
inspection the palate is seen to be lower than normal, perhaps on one 
side a little more than on the other, and it does not draw up as it 
should when the patient utters the sound "ah." Its sensibility is dimin- 
ished or lost and no reflex response can be obtained through it. If the 
disease is prolonged the palatal muscles will be seen to be distinctly 
atrophied. The majority of these cases get well within a few weeks. 

Next to the paralysis of the palate, both in the time of its appear- 
ance and the frequency of its occurrence, is the paralysis of the mus- 
cles of accommodation. Tn many cases, with or without the implica- 
tion of the palate, the patient complains of diminution of vision for 
near objects while it may be normal or even increased for far objects. 
In the fact that this cycloplegia often precedes the palsy of the palate 



THE NON-NEURONIC DISEASES 6oi 

and is in all probability due to nuclear degeneration, the generalized 
nature of the intoxication receives support. The reactions of the pu- 
pil are generally normal. It may be sluggish to light, but is scarcely 
ever lost. It may contract when an effort is made to accommodate 
even though the accommodation is absent. Sometimes the external 
ocular muscles are involved. Any of the remaining cranial nerves may 
be affected. Immobility of the epiglottis from implication of the su- 
perior laryngeal nerves makes swallowing a difficult and dangerous 
task for fear of food getting into the trachea. Paralysis of the vocal 
cords through the involvement of the inferior laryngeal nerve causes 
hoarseness of the voice and even aphonia. Disturbances of the respira- 
tory and cardiac functions are particularly to be dreaded. These are 
not rare and often are the cause of death. Though the ophthalmoscope 
reveals no morbid changes, a concentric contraction of the fields of 
vision, marked, of course, by the effect of the cycloplegia, has been occa- 
sionally seen. Hearing seems never to have been affected, but taste and 
smell have. The tongue and face are rarely ever paralyzed. 

In many patients paralysis in the limbs follows the above manifes- 
tations. It may come on while the cranial palsies are still existent or 
after they have begun to clear up. Weakness, paresthesias and pains 
are first complained of in all four extremities. This quadriplegia is 
the indication of the polyneuritic character of the trouble. The legs 
more often suffer before the arms. The muscles are soft and flabby. 
The reflexes are diminished or lost. The electrical reaction of degen- 
eration is present and there is some atrophy. In a word, the paralysis 
is of the typical flaccid, progressive, degenerative type. As it involves 
the extensors and flexors of the limbs about equally, there are no de- 
formities. Walking is impaired or rendered impossible. The sensory 
manifestations with an ataxic gait may lead to a mistaken diagnosis 
of locomotor ataxia if the history and entire course of the disease are 
not given careful consideration. 

Not often are the trunk muscles involved, and yet they may be so 
weak that the patient cannot turn over in bed, or the respirations may 
be embarrassed, or it may be impossible to hold up the head. The 
diaphragm may cease to act. 

The prognosis of diphtheritic paralysis is particularly favorable 
if deglutition is not too much interfered with and the respiratory and 
cardiac functions continue intact. The local forms of the disease usu- 
ally get well in a few weeks; the generalized forms attain their maxi- 
mum in about two or three months and then rapidly decline, the aver- 
age length of time being three months. Recovery, as a rule, is com- 
plete, though in exceptional cases certain muscles may remain par- 
tially paralyzed. Dangerous symptoms arc paralysis of the vagus nerve 
and of the respiratory muscles, particularly the phrenic. 

Myocarditis and cardiac paralysis arc not unfrequent and fatal 
occurrences. Death by inanition has occurred in deglutitory paralysis. 
Severe cases when fatal die early; others run an irregular course with 
what seems like a series of relapses and then die of cardiac or respira- 
tory paralysis. In every case the prognosis is uncertain and especially 
so if there is involvement of the trunkal musculature. 



602 



THE NOX-NEUROXIC DISEASES 



Antitoxin treatment of diphtheria does not seem to have lessened 
the relative frequency and severity of the subsequent paralysis ; though 
it is claimed by Lublinski and some others that the generalized form 
is seen more frequently without the preceding localized form. 

(b) Rheumatic Type. — Polyneuritis sometimes occurs in con- 
nection with rheumatism. It is rare, but such cases have been reported 
by Putnam, Dana, Gowers, Remak and others. I have under observa- 
tion now an ataxic case due solely to rheumatic polyneuritis. Paralysis 
of neuritic origin not uncommonly occurs in the joints that are in- 
flamed and swollen, especially the ankle joint. The exact relationship 
of the arthritis to the neuritis is not clear. Some hold that it is infec- 
tious, others that it is purely mechanical and irritative. The symptoms 
of the neuritis are typical. Thus in a patient reported by Gowers and 
seen by Remak there was subacute articular rheumatism of both ankle 
joints with considerable pain and later on incomplete palsy of all four 
limbs, partial atrophy of the muscles with the reaction of degenera- 
tion, absence of knee-jerk, tremors and involuntary twitchings and 
disturbances of sensibility. The generalized nature of the trouble was 
still further emphasized by the implication of the face and facial 
nerves and the existence of some optic neuritis. This picture is dupli- 
cated by my case. The modern view that acute articular rheumatism is 
primarily a general infection would seem to receive some support from 
the occasional occurrences thus of polyneuritis with it. 

(c) Puerperal Type. — This has only been recognized the last 
few years. It may occur during pregnancy, especially in those who 
suffer from excessive vomiting. It is due to septic infection and ap- 
pears in both the localized and generalized forms. In the former the 
ulnar and median nerves are the affected nerves of choice. Some- 
times particular nerves in the lower limbs are similarly affected. In 
the generalized form of the trouble all of the peripheral nerves of the 
limbs, and any of the cranial nerves, are affected. Optic neuritis has 
several times been seen. In some cases the clinical picture corresponds 
quite a little to Landry's paralysis. 

(d) Other Types. — Almost any form of general infection seems 
capable of setting up a general neuritis. As the bacilli themselves do 
not provoke the lesion, but rather their poisonous products, these post- 
febrile cases correspond with those that result from alcohol and the 
metallic poisons. The lesion is toxic in origin, of wide distribution and 
degenerative in character. Owing to some obscure influence, the differ- 
ent infections give rise to some slight differences in symptomatic de- 
tails, justifying somewhat the use of the term types of polyneu- 
ritis in connection with them. For example, typhoid infection of the 
nervous system shows itself more prominently in brain symptoms and 
paraplegic weakness.. The same is true of typhus fever, though the 
paraplegic weakness and the more pronounced signs of poliomyelitis 
are less common. Variola is characterized more particularly by spinal 
manifestations along with the neuritic. Spinal symptoms are rare 
after scarlet fever, whereas cerebral trouble with non-nephritic neuro- 
retinitis is not uncommon. Many of the symptoms of influenza are 
undoubtedly due to a mild generalized polyneuritis which in some re- 



THE NON-NEUKONIC DISEASES 603 

sj>ccts resembles post-diphtheritic neuritis. Mumps, dysentery, erysip- 
elas, pneumonia, malaria, gonorrhoea and purulent pleuritis have ail 
been followed by neuritis of a more or less disseminated and degener- 
ative type. Pure peripheral neuritis, especially of the lower limbs, has 
been observed symptomatically during life and microscopically after 
death in tuberculous patients. The rarity of true syphilitic polyneu- 
ritis has caused some to doubt its existence. I have seen it, however, 
though I am inclined to question whether it ever occurs without some 
implication of the brain and cord. If it be true, as Savage and others 
contend, that syphilis never attacks the neurones themselves, then we 
must look to the nutritive disturbances of the cells in the cord through 
the specific arteritis or to the compression of the spinal roots by the 
specific meningitis to explain the degeneration of the peripheral nerves 
in tabes, in pseudo-tabes and specific polyneuritis generally. Diabetic 
polyneuritis is characterized by an atrophic paralysis, but especially 
by the severity of its sensory symptoms. The weakness complained of 
in the lower extremities is mostly due to implication of the crural, 
obturator and peroneal nerves. The eye symptoms and visual dis- 
turbances in diabetics have long been recognized. I have a diabetic 
under observation in whom paresis of the lower extremities, optic 
neuritis, unilateral facial numbness, pains and paraesthesiae in various 
parts of the body, especially about the lips and herpetic eruptions upon 
the skin of the forehead, have all appeared in a remittent sort of a 
way. On account of the prominence of the sensory disturbances in 
these cases a pseudo-tabes may appear and be confused with locomotor 
ataxia. The prognosis of this form of neuritis is usually favorable. 

Of great interest, especially to tropical practitioners, are the en- 
demic forms of polyneuritis. We do not know much about these 
though it is generally accepted that they are due to an infective agent 
belonging to certain localities. They occur endemically and epidem- 
ically. Beriberi, sometimes called kakke and found especially in Japan 
and along the east coast of Africa, is a form of infectious polyneuritis 
in which the heart and blood-vessels seem to be particularly involved. 
The cranial nerves usually escape, except the pneumogastric. The in- 
tellectual and emotional centers remain untouched. Trophic skin symp- 
toms are exceedingly rare or entirely absent. Dropsy is a constant 
manifestation. In the early stages of the disease the specific gravity 
of the urine is always low, then it rises, and finally ends by going above 
tin- normal. There are no particularly abnormal elements in the mine. 
Tin- mortality rate under certain conditions is very high. The general 
infections character of the trouble is shown by the indication of spinal 
cord lesions in the zone-like distribution of the anaesthesia along with 
the polyneuritis symptoms. The old view that the eating of rice con- 
stituted the most important etiological factor in the disease has been 
seriously shaken by some recent careful observations and experiments. 
Some authorities believe that a form of malarial poisoning is the real 
agent in the production of the disease. Glogner and others claim that 
they have found in the blood of these patients malarial plasmodia nr 
similar organisms. 

. \katama is a form of endemic peripheral neuritis found in West 






604 THE NON-NEURONIC DISEASES 

Central Africa, of obscure origin and characterized by numbness, prick- 
ling and burning sensations in the presence of cold or damp. It is 
found in all ages and both sexes, but more often in men than in women, 
in the young and middle aged than in the old, and never in children or 
Europeans. The symptoms are all indicative of a mild generalized 
neuritis. Prognosis is good as to life, but uncertain as to relief. After 
years of suffering the trouble sometimes ceases spontaneously. 

Leprous polyneuritis is an endemic, specific form of the disease. 
The cause of the disease is the bacillus of leprosy and the pathogenesis 
of the nervous manifestations is a toxic peripheral neuritis. The bacil- 
lus is abundantly found, as I have seen, in the diseased nerves. The 
neuritis seems to be of the primary interstitial type, though it is an 
open question whether the parenchymatous degeneration is due sec- 
ondarily to mechanical compression by the inflamed interstitial tissue 
or primarily to the poisonous products of the bacilli. The symptoms,, 
motor, sensory and trophic, with the sensory predominating, are all 
typical of a peripheral multiple neuritis. 

DiAGNOSis.-^-Generally the diagnosis of multiple neuritis is not 
difficult. A careful consideration of the etiological factors in the case, 
the mode of origin and general course of the disease, the character and 
distribution of the symptoms goes far in establishing it. The entire 
clinical picture exhibited by the patient and not one or two symptoms 
alone must be studied if mistakes are to be avoided. There are two 
features in the clinical picture which, when taken in conjunction, will 
make the diagnosis absolutely positive. In the first place, one must 
discover the cardinal indications of a peripheral neuritis or degenera- 
tion, disease of the lower neurones. These consist of flaccid motor 
paralysis, loss of deep reflexes, muscular atrophy, certain trophic mani- 
festations, electrical reaction of degeneration and sensory phenomena 
of a variable character. The details in regard to these symptoms have 
been considered in the symptomatology. In the second place, the wide 
distribution of these symptoms must be noted and their relatively irreg- 
ular severity within this wide area of distribution. A progressive quad- 
riplegia, involving more or less symmetrically first the ends of the lower 
limbs and then the upper, with cutaneous patches of hyperesthesia, 
anaesthesia, hyperalgesia and analgesia, is pathognomonic. 

If the above facts are kept well in mind, the differential diagnosis 
between polyneuritis and acute anterior poliomyelitis, ascending 
myelitis, tabes dorsalis, spinal meningitis and hemorrhage is not diffi- 
cult. 

In acute anterior poliomyelitis the age of the patient, the initial feb- 
rile disturbance and the course of the disease are quite different. In 
infantile palsy there is apt to be a recession of the symptoms from an 
initial wide extent of them; in polyneuritis, the trouble usually begins 
in a limited area and rapidly extends. In the former, especially after 
the symptoms have begun to recede, there is a remarkable limitation of 
the paralysis to individual muscles and muscle groups, whereas in the 
latter much larger groups or even the whole limb is gradually involved 
in the paralysis. In poliomyelitis the atrophy is somewhat more rapid 
and severe, especially in particular muscles. Moreover, the damage is 



THE NON-NEURONIC DISEASES 605 

more permanent than it is in multiple neuritis. There are no sensory 
phenomena, as in the latter disease, nor are the cranial nerves ever im- 
plicated. The symmetrical distribution of the symptoms, their pro- 
gressive character, the presence of sensory phenomena, and the impli- 
cation of the cranial nerves establish the diagnosis of neuritis posi- 
tively in contradistinction to poliomyelitis. It does not follow, however, 
that there may not be some poliomyelitic manifestations along with the 
neuritic. As I have pointed out in connection with the toxic and in- 
fectious cases, the disease process is an extensive one and it is probable 
that some of the peripheral degeneration is due to damage to the cells 
in the gray matter of the cord. In these cases, however, there is always 
some primary disease of the peripheral nerves also, and on account of 
this the local tenderness of the nerves and muscles proves the presence 
of the polyneuritis. If inflammatory alterations of the optic nerve can 
be detected, the case is positively one of peripheral neuritis. 

In myelitis the symptoms are more distinctly paraplegic in char- 
acter, with involvement of the rectal and vesical sphincters. There is 
present a girdle-pain and the sensory phenomena generally tend to- 
wards anaesthesia. In myelitis high up in the cord the reflexes are 
exaggerated, the muscles more or less rigid and later on contractured. 
The muscular atrophy is not so distinct, whereas the cutaneous trophic 
symptoms are more pronounced. The electrical responses are not much 
altered. 

In spinal hemorrhage and meningitis the character of the pains 
and their distribution about the trunk, as well as the limbs, the local 
tenderness in the spine, the inclination towards opisthotonos, the in- 
volvement of the sphincters and the absence of cranial symptoms, 
make the diagnosis clear. 

The sensory types of multiple neuritis may easily be mistaken for 
tabes dorsal is, for the ataxia, the pains, the absence of the reflexes and 
even some of the trophic symptoms are the same in both. Pseudo-tabes 
is an excellent name for these neuritic cases on account of this close 
similarity. The differential diagnosis in a few exceptional cases is 
absolutely impossible. The following points, if carefully noted, will 
help to distinguish one disease from the other in most of the cases: A 
history of syphilis is obtained in most of the cases of locomotor ataxia. 
The existence of a true syphilitic polyneuritis is open to question. In 
the history of multiple neuritis toxins play the greatest role, and after 
them the infections of a severe and acute character. In tabes dorsalis 
the symptoms approach gradually and several years after the primary 
infection ; in pseudo-tabes the onset of the symptoms is rather abrupt, 
their extension is rapid, and their distribution includes generally all 
four extremities early and equally. The ataxia in polyneuritis is not 
so distinctly sensory as it is in tabes; it is a little more paralytic in 
character. The Argyll-Robertson pupil is not a symptom of multiple 
neuritis and the early bladder troubles of tabes are rarely complained 
of in polyneurites. Local tenderness upon pressure is not found in 
tabes, whereas it is all but pathognomonic in multiple neuritis. The 
crises, especially the gastric crises, are not symptoms of the latter. 
The trunkal anaesthesia of tabes is practically unknown in polyneuritis. 



6o6 



THE NON-NEURONIC DISEASES 



The progressive and incurable character of tabes is to be contrasted 
with the curability of polyneuritis and its tendency after a short time to 
get well. 

Treatment. — The results of the proper treatment of multiple 
neuritis are among the happiest that are to be attained in neurology.. 
A clear recognition of the origin, nature and stage of the disease is a. 
sine qua non, however, of its successful management. The diagnosis- 
having been positively established, the first thing to do is to secure the 
patient's entire confidence and co-operation and to impress upon him the 
favorable character of the prognosis if he is hopeful and submissive. 
It is well to explain very clearly to him that the greatest danger of a 
fatal issue lies in the possible implication of the cardiac and respiratory 
nerves, and that this is to be avoided by perfect serenity of mind and 
quietude of body. It is also well to prepare his mind by telling him that 
the disease usually increases in severity, though not necessarily in ex- 
tent, for the first four or five weeks, then remains stationary with now 
and then a possible slight relapse for a month or two longer, and 
finally disappears in the course of several months more or a year. The 
avoidance of surprises, disappointments and rebellious opposition as a 
result of this forewarning is to me a desideratum of much more con- 
sideration than is the momentary chagrin and depression on the part 
of the patient when he learns of the prolonged course of his disease. 
Most patients when thus reasonably appealed to, respond heartily to 
all that is about to be done for their restoration to< health. If, however, 
they revolt against the physician's advice, decline his further ministra- 
tions and undertake a line of treatment and a mode of life which may 
hasten a fatal termination, the physician will escape all blame in the 
matter. 

The two cardinal factors^in the management of multiple neuritis 
are to remove the cause and to put the patient at absolute rest. No 
compromise can be allowed in regard to these. 

In the removal of the cause both passive and active therapy may 
be necessary. Unless the heart is too weak, all alcoholics should be at 
once discontinued. In some cases the alcohol can only be diminished. 
The amount of the diminution can only be determined and regulated by 
a careful observation of the pulse in each individual case. It is not 
well therefore ever to suddenly deprive a patient with alcoholic poly- 
neuritis of all stimulus. A much safer way would be to gradually re- 
duce the alcohol, rapidly in some cases and more slowly in others, but 
always as promptly and completely as possible, and to gradually in- 
crease the administration, pari passu, of some other form of stimulant, 
like strychnia, ammonium salts, etc. 

If the disease is due to lead, arsenic, copper, mercury or other 
toxic agent, of course the source of the poisoning must be sought for 
and eliminated at once. The iodide of potassium will help to remove 
the lead from the body. Whatever the toxic substance may be its 
elimination from the organism should be hastened by free purgation, 
diuresis and diaphoresis. Free bathing is excellent for this purpose, 
but it must not cause too much exertion on the part of the patient. 

The infection that may lurk behind the multiple neuritis calls for 



THE NON-NEURONIC DISEASES 6oj 

its own appropriate therapy. Quinine must be given when there is 
malaria present. Antistreptococcic serum may be tried in scarlatinal, 
puerperal and other forms of septic polyneuritis. The salicylates are 
indicated in rheumatic neuritis. Autointoxication with treatment di- 
rected to the alimentary canal must be thought of. Endemic cases of 
the disease, like beriberi, must be removed from the infected locality 
and the latter cleaned up as far as possible with bactericides. Severe 
anaemia, cachexia and senility with arterio-sclerosis, with which poly- 
neuritis is sometimes associated, call for their own special treatment. 

If there is a history of syphilis preceding the neuritis, one natural- 
ly thinks of the administration of mercury. It is well to try the 
remedy, but it must be done very cautionsly. It is not positively set- 
tled yet whether the polyneuritis that sometimes occurs in syphilitics is 
due to the infection or to the heroic use of mercury, which in most 
of these cases will be found to have just preceded the onset of the 
paralysis. In my own opinion the polyneuritis is due to the syphilis 
and not to the mercury, reasons for which belief I will not stop here 
to elaborate. Nevertheless I am convinced from personal observation 
that the administration of mercury may render the multiple neuritis 
decidedly worse. Therefore, if there is no improvement, and especially 
if the symptoms are increased by the cautious use of mercury- in poly- 
neuritis in a syphilitic patient, it had better be promptly discontinued 
and the iodide of potash used instead. 

If the case is a severe one, absolute quiet, both of mind and body, 
is imperative. The paralysis will usually effect the physical rest; the 
mental calmness must be secured by seclusion and appropriate diver- 
sion. Hence in the early stage of the disease these patients had better 
be placed in a hospital where they can be kept apart from all domestic 
and business intrusion, or if they must remain at home, they should 
be given a firm and tactful nurse and isolated in some remote apartment. 
It is more difficult to manage in this respect the milder cases, for they 
will insist upon moving about some in their partially paralyzed condi- 
tion. They must be enjoined to keep their bed and only move for the 
sake of change from the bed to the couch or rolling chair. In a word, 
all active functioning of the nervous system must be prohibited during 
the first two or three weeks of the disease. Nor must there be any 
passive activity, such as massage, hauling of the patient about, etc., 
during this same period. If immobility and mental rest are accom- 
plished in the beginning of the disease and the cause promptly removed, 
it will cease that much sooner to extend and the stationary and con- 
valescent period will be that much earlier secured. It must never for a 
moment be forgotten that the cardiac and respiratory functions are 
liable to be affected in any case and to avoid this danger the rest 
must be almost absolute. The patient must not move about in bed 
hastily, or sit up, until all acute symptoius show signs of abating. Even 
then caution must be observed. 

In the first stage diaphoretic measures . if used carefully, may be 
highly advantageous. Hot baths, hot packs fostering perspiration for 
an hour or two daily or every other day, may be employed. The heart 
action must be closely watched. Hot drinks may be of some benefit in 






6o8 



THE NON-NEURONIC DISEASES 



provoking diaphoresis and diuresis, with or without the hot baths. In 
one or two instances I have seen the disease increased and extended 
by the too vigorous use of heat in this way. Cold is always contra- 
indicated, hence the room must be kept warm and free from draughts. 

The weakness and pains are two of the most prominent symptoms 
calling for special attention. The former is to be combated by a 
strengthening and nutritious diet and by the appropriate use of stimu- 
lants. Milk in abundance, egg-nog, meat juices, tender beef, fats and 
ood-liver oil are to be given as freely as the digestive organs will dis- 
pose of them. Diphtheritic patients may have to be fed through a tube. 
For the weakness it may be necessary to resort to wine, strychnia, 
camphor, aromatic spirits of ammonia, etc. The shooting pains and 
muscular tenderness are often so marked that relief, however slight, 
must be attempted. For this purpose the salicylate of soda, in twenty- 
grain doses every two or three hours, is sometimes useful. Dana says 
that a dram or two of the fluid extract of ergot repeated in three hours 
sometimes relieves the pain. The coal-tar preparations have not been 
very effective in my hands and I am loath to push them on account 
of their depressing action upon the heart. I prefer the use of warmth, 
such as swathing the limbs in hot flannels and in cloths wrung out in 
hot water. Painting the limbs with menthol and enveloping them in 
cotton batting is sometimes soothing. As a last resort morphine may 
be used. 

When the diminution of the pains indicates that the disease has 
entered upon its stationary or convalescent stage, massage, electricity 
and measures to counteract late contractures and deformity are to be 
instituted. If there are any signs of irritation remaining, galvanism in 
the form of a stabile current is the only form of electricity permissible. 
Later on the labile current, in strength of five to eight milliamperes, 
may be administered daily for about five minutes. The faradic current 
to stimulate the muscles should only be employed when convalescence 
has gotten well under way. Much more effective than electricity in 
my experience has been massage. The muscles should be gently rubbed 
and kneaded and stroked once or twice a day for a short time. The 
use of olive oil or cocoanut oil in the hand of the masseur is agreeable 
to the patient. The stroking should be gentle, towards the body and in 
the vicinity of the principal nerves affected. It may be increased in 
vigor as the case continues to improve. Passive exercises and mild 
gymnastics may later on take the place of the massage. Exhaustion* 
must be carefully guarded against in all these mechanical measures and 
the patient should be urged to lie down and rest frequently. Tonics, 
such as strychnia, arsenic, iron, quinine and the hvpophosphites, are to 
be administered. In obstinate paralysis Oppenheim recommends the 
subcutaneous administration of strychnia, one-sixtieth to one-twentieth 
grain several times daily. Iodide of potassium, two per cent, carbolic 
acid and carbolmorphine, the latter two hypodermically in the neighbor- 
hood of the affected nerves, have received high endorsement. In ad- 
vanced convalescence general tonic and hygienic measures, including 
baths, change of climate, abundance of fresh air, good food and judi- 
ciously guarded exercise are to be recommended. 



THE NON-NEURONIC DISEASES 609 

Deformities, particularly in young persons, are to be prevented bv 
watching the attitude of the limbs during the course of the disease. 
When late contractures begin to manifest themselves they are to be 
combated by massage, passive motion, forcible replacement with the 
appropriate use of splints and other apparatus. Tenotomy is not de- 
manded here, as it often is in poliomyelitis, for the disease being more 
generalized opposing sets of muscles are apt to be more equally af- 
fected. 

Relapses are to be warned against and prevented by a strict ad- 
herence to the directions of the medical adviser. 

TUMORS OP THE NERVES. NEUROMATA. 

A neuroma in the modern sense is a nerve tumor, but not all nerve 
tumors are neuromata. Since the discovery of Virchow that there are 
specific nerve newgrowths, and newgrowths in the nervous system that 
are not specifically neural, neuromata have been divided into the true 
and the false. It is but fair to say that some pathologists do not accept 
the distinction thus made by Virchow. 

The true neuroma is very rare and consists of true nervous ele- 
ments. Virchow speaks of the "myelinic" and "amyelinic'' forms, those 
that contain respectively medullated and non-medullated fibres. Ziegler 
is among those who doubt the propriety of separating the neuromata 
into a special class and believe that the nerve-fibres are not implicated 
in the neoplasm. He thinks the growths are merely neurofibromata, neu- 
rosarcomata, neurolipomata, etc., arising in the epineurium and peri- 
neurium. 

The false neuromata are heterologous growths and are given the 
same names that they would have were they in other parts of the body. 
They include the fibromata, sarcomata, myxomata, syphilomata, etc. 
The first are the most common and are the basis probably of the 
majority of the true neuromata. There is nothing distinctive about 
these false neuromata that need special notice because they happen to 
occur in the nervous system. 

Neurone cell-bodies have scarcely ever been discovered in the true 
neuromata. Between the nerve fibres there is connective tissue which 
renders the growth hard and firm and which is ofttimes so abundant 
that the neoplasm stands midway between the true and false neuro- 
mata. These tumors are multiple or single. They occur mostly on 
tin- spinal nerves and are usually small, varying in size from a pea to a 
pigeon's tgg ( i cm. to 6 cm.). They are prone to appear as multiple 
growths in particular nerve areas. For example, the brachial plexus, 
the cauda equina or the nerves of the pelvis may be the seat of them. 
Sometimes they are strung along the nerve trunks like beads. 

Multiple neuromata are of the neuro- fibroma-tons variety. Tlie\ 
are exceedingly numerous sometimes, as many as a thousand or more 
having been counted in one individual. 

Fibroma molluscum multiplex, a general neurofibromatosis, is the 
condition in which multiple neuromata are found upon the trunks of the 






6io 



THE NON-NEURONIC DISEASES 



subcutaneous nerves. Nsevi are generally associated with it, thus 
indicating the congenital nature of the trouble. 

Plexiform neuroma, or congenital elephantiasis, is where there 
is a great interlacing of cords, nodular and tortuous. The fibres of the 
nerves, as for example, the trigeminal, the lumbar, the brachial and 
solar plexuses, the nerves of the penis and mammae, thicken, break up 
and recombine in a twisted sort of a way. They can be felt plainly 

FIGURE 133. 




General ueurofi- 
bromata. Rosary-like 
arrangement of the 
neuroma along the 
peripheral nerves of 
the right arm; the 
small knots areplainly 
visible beneath the 
skin. (After Robert 
Smith, reproduced by 
Marie.) 

under the skin. The nerve-fibres are united by the hyperplastic con- 
nective tissue. The disease begins in foetal life and is related to 
pachydermatocele and elephantiasis mollis. The growth of this condi- 
tion is extremely slow. It exerts pressure upon the neighboring struc- 
tures. 

Sometimes multiple neuromata are malignant. Trauma and hered- 
ity are behind them and the greater nerve trunks are the seat of them, 
especially the perineurium. They are spindle-shape and sometimes are 
very large in size. Sarcomatous cells are often found in them. 



THE NON-NEURONIC DISEASES 6ll 

Tubercula dolorosa are small multiple tumors, mostly of the fibro- 
matous variety, that occur in great profusion on the subcutaneous 
sensory nerves. They are painful and can easily be felt. 

Gliomata are not frequently seen in the peripheral nerves. They 
occur in the auditory nerve. 

Carcinoma usually occurs as a secondary condition in the form of a 
diffuse or nodular infiltration of the nerve from a neighboring growth. 
Rarely it is seen as an isolated neoplasm. 

Syphilomata occur mostly on the cranial and spinal nerve roots ; 
not so often on the peripheral nerves. 

In lepra ancesthctica the nerves are often infiltrated, to a very great 
degree, causing neuro-fibromatous swellings upon them. The condi- 
tion is of the nature of a cirrhotic inflammation rather than a nodular 
development. 

Nerve tumors are practically always within the nerve sheath. If 
they are on one side, the nerve itself may pass intact around them. 
Frequently, however, the nerve is involved and infiltrated, with its 
fibres spread out over the surface of the growth. Even under these 
circumstances the nerve may not be much damaged, which explains the 
frequent absence of symptoms. False neuromata are more damaging 
to the nerve fibres and are therefore accompanied by more pronounced 
symptoms than are the true neuromata. 

Etiology. — The etiology of tumors has not been brought to com- 
pletion yet. Heredity and a neuropathic constitution are undoubtedly 
responsible for certain types of them, and to some degree for all of 
them. This is shown in their familial characteristics and their frequent 
association, especially the multiple neuromata, with idiocy and cretin- 
ism. The phthisical and scrofulous condition were thought by Virchow 
to be blameable for them. Curiously the multiple variety of the disease 
- eems to belong to men, the isolated to women. Age exercises no in- 
fluence upon their appearance. Even the hereditary form of the dis- 
ease may not appear till middle age. 

The cachexia: give rise to, and determine, the character of the 
neoplasms. Whatever underlies in the patient's constitution the forma- 
tion of the fibrous growths, sarcoma, carcinoma, myxoma, lipoma, tuber- 
cle, is responsible for the same conditions in the nervous system. 
Traumata and chronic neuritis may initiate the neuromata. Amputa- 
tion neuromata, or so-called bulbous nerves, belong here. As the nerve 
fibrillar, when cut, grow out from the proximal end like the twigs of .1 
vine, it i> easy to understand how by mechanical obstruction and other- 
wise they may become twisted and agglutinated together and held h\ 
the connective tissue in a ma>>. 

Symptoms. — I have already remarked that as the nerve often 
courses intact around the tumor, there arc- n<> neural symptoms of its 
presence. ( )n the other hand, the symptoms may be most severe and 
even dangerous, the latter when the growth are in such nerves as the 
pneumogastric, phrenic or other splanchnic nerve. The symptoms are 
of an irritative or paralytic character and involve all neural functions, 
motor, sensory, trophic, vasomotor and secretory. In a word, they are 
the symptoms of neuralgia and neuritis. 



I * 



6l2 THE NON-NEURONIC DISEASES 

Pain is a particularly common symptom. It may be a local tender- 
ness or a peripheral sharp, shooting pain. Often it is acute, burning, 
boring and darting. It follows the course of the nerve or appears in 
the area of its distribution. In the same area paresthesia occur and 
more or less hypcusthesia. The topographical correspondence of these 
sensory phenomena with the motor manifestations is a particularly 
characteristic feature. 

The mot or phenomena include twitchings, jerkings, spasms and 
tonic contractions in the muscles innervated by the diseased nerve. 
Paralysis and atrophy are very rare. General convulsions and reflex 
epilepsy have been seen ; also hysteria, neurasthenia and hypochondria- 
sis. The pain is the most disturbing feature, often completely wearing 
the patient out and reducing him physically. 

In general neurofibromatosis Marie has noted the occurrence of 
psychosis, sensory disorders and convulsions. 

Paraplegia and vesical paralysis sometimes are the result of neuro- 
mata of the cauda. 

Plexiform neuroma rarely produces any other symptom than a 
hypaesthesia. 

Prognosis. — Neuromata are progresssive, though they may be- 
come stationary or regress. Multiple neuromata offer a better general 
prognosis than do the isolated neoplasms. The reason is obvious. 
Multiple neuromata are usually fibrous. Among the isolated tumors 
occur the heterologous growths, such as sarcoma, cancer, etc. The 
presence and the severity of the symptoms add to the gravity of the 
prognosis. 

Treatment. — Except in syphilomata, when, of course, mercury 
and the iodides are called for, medicines are useless in tumor of the 
nerves. The condition is essentially a surgical one. Of course, this 
applies to isolated tumors that can be reached and that reveal symptoms. 
After extirpation of a neuroma, the possibility of complete paralysis 
is great. This can be obviated sometimes by an immediate suturing, 
transplanting or other form of operation upon the nerve stumps. Some 
tumors can be peeled off; as it were, from the nerve. and when thus re- 
moved there will be a restoration of the neural functions. This has 
happily occurred several times. 

In cases of multiple tumors some of the growths with marked symp- 
toms can be operated upon. Return of them is the rule, however. 

Electrolysis and caustics are inadvisable. There is danger of 
setting up neuritis and making what is bad worse. Strong galvanic 
currents applied percutaneously, mercury and large doses of iodides 
have been recommended' for true neuromata and neurofibromata. The 
results of the treatment, however, are not very encouraging. 

The terminal neuromata of tubercula dolorosa max he cut out 
without danger; otherwise these and all painful tumors must needs 
be quieted with analgesics. 

There is no treatment for plexiform neuroma. Excision is inad ■ 
visable. 



THE NON-NEURONIC DISEASES 613 

DISEASES OF THE SPINAL NERVES. 
PHRENIC NERVE. 

Diaphragmatic paralysis is usually clue to spinal cord disease. Dis- 
ease that involves the third and fourth cervical roots implicates the 
phrenic nerve. It need hardly be mentioned that such diseases include 
spinal meningitis, particularly pachymeningitis, caries of the spine, 
fractures, dislocations, exostoses, tumors, hemorrhage and especially 
gummatous meningitis. Direct traumata do not often reach the nerve, 
because it is very deep in the neck. Wounds in the neck and tumors 
and aneurisms in the thorax may implicate it. Duchenne has met 
with disease of the nerve in lead poisoning. It has been affected 
bilaterally in alcoholic intoxication. Diphtheria has infected it. Trie 
influence of cold in setting up a phrenic neuritis should be regarded 
with skepticism. 

Paralysis of the diaphragm is, of course, the symptom of phrenic 
nerve disease. If one nerve is implicated, one side of the diaphragm 
only is paralyzed. The continued activity of the other side, however, 
causes the whole muscle to move so that it is often difficult to discover 
the unilateral paresis. 

In a state of quietude on the part of the patient, the loss of 
diaphragmatic stimulation does not materially lower the breathing ca- 
pacity. Exertion, however, causes quick breathing and a weakening 
of the voice. This dyspnoea may become very pronounced and dis- 
tressing. Both inspiration and expiration are affected. The movements 
of the thorax are usually increased, the upper part of the abdominal 
wall being so much drawn forward as to simulate the effect of the 
descent of the diaphragm. 

Paralysis of the diaphragm produces trouble in diagnosis only 
when it is unilateral. In most forms of phrenic neuritis it is unilateral. 
It is bilateral generally in spinal cord diseases dM(\ diseases of the spine. 
Careful examination will enable one to detect a unilateral paralysis. 
The breathing sounds at the base of the lung upon that side will be 
diminished. The electrical responses will be diminished. The objective 
diaphragmatic phenomenon will be absent. And there may be a painful 
spot to pressure on the scaleni muscles near the sterno-mastoid muscle. 

Sometimes the diaphragm is paralyzed from myositis. This may 
lead to an erroneous diagnosis of phrenic neuritis. It is usually a 
secondary trouble from peritonitis or pleuritis, on account of which 
it can usually be readily differentiated. The- characteristic pains of 
these latter diseases arc- also distinguishing. 

It is very doubtful if there is a true hysterical diaphragmatic 
paralysis. Superior COStal breathing is more common in women than 
in men and it is the type of respiration in nervous people and hysterics. 
It is easy, therefore, for a hysteric to simulate diaphragmatic paralysis. 
Mental distraction will cause the epigastrium to advance and thus show 
the absence, when a deep inspiration is unguardedly taken, of a true 
organic paralysis. Dyspnoea docs not occur in hysterics. Ether nar- 



614 



THE NON-NEURONIC DISEASES 



cosis would confirm the diagnosis. According- to Wernicke, there is a 
hysterical insufficiency of the phrenic nerve which is associated with 
fear and inspiratory dyspnoea. 

Callender has described a primary and isolated degeneration of 
the diaphragm after death. Whether it ever produces inaction of the 
muscle during life we do not know. In spinal cord disease that causes 
diaphragmatic paralysis, other muscles are svmptomatically affected 
also. 

The prognosis is generally favorable, though it is dependent upon 
the cause. Multiple neuritis as a cause offers a rather unfavorable 
prognosis. I have seen dyspnoea and death occur in this disease in this 
way. 

The treatment involves first the removal of the cause. Counter- 
irritation over the anterior triangle of the neck and electrical stimula- 
tion of the nerve when inflammation has subsided, about sums up the 
therapy. Strychnia has been especially commended in the diphtheritic 
paralysis. 



THE BRACHIAL PLEXUS. 

Anatomy. — The brachial plexus is formed by the union of the an- 
terior trunks of the four lower cervical and the greater part of the first 
dorsal nerves. It reaches from the lower part of the neck to the axil- 
lary space. Opposite the coracoid process it ends in the large nerves 
that go to supply the upper extremity. 

The fifth and sixth cervical nerves join together at the outer bor- 
der of the scalenus medius to form an upper trunk. The eighth cervical 
and first dorsal form in the same way a lower trunk. The seventh 
forms the middle trunk between these two. Just outside of the scaleni 
muscles, each primary trunk divides into an anterior and a posterior 
branch. The anterior branches of the upper and middle trunks unite 
and form the upper or outer cord of the plexus. The anterior branch 
of the lower trunk alone forms the lower or inner cord of the plexus. 
The posterior branches of all the three trunks unite to form the middle 
or posterior cord. 

The branches that come off from the brachial plexus are very 
numerous. Those that originate above the clavicle are the posterior 
thoracic and the suprascapular nerves, a nerve for the rhomboid mus- 
cle, another for the subclavius, branches for the scaleni and longus colli 
muscles and sometimes a branch to the phrenic nerve. Those that 
originate from the plexus below the clavicle may be arranged as fol- 
lows, according to Quain, whom I follow in these anatomical facts : 

From the upper or outer cord — the external of the two anterior 
thoracic nerves, the muscido-cutaneous, and the outer head of the 
median. 

From the lower or inner cord — the inner of the two anterior 
thoracics, the nerve of Wrisberg or small internal cutaneous, the in- 
ternal cutaneous, the ulnar and the inner head of the median. 

From the posterior cord — the subscapular nerves, the circumflex 
and the musculo-spiral. 



THE N0X-XEUR0X1C DISEASES 



615 



For the spinal segmental origin and the ultimate distribution of 
the branches of the brachial plexus, the reader is referred to the admira- 
ble tables compiled from Starr, Mills. Sachs, Dana and Thorburn at 

FIGURE 134. 

Diagrammatic 
outline of the cervical 
and brachial plexuses. 
(A. T.) 4 

The nerves are separated 
froin the spinal cord at their 
origin and are supposed to 
be viewed from before : CI, 
the first cervical or sub- 
occipital nerve, and the 
It oman numbers in succes- 
sion from II, to VII i, the cor- 
responding cervical nerves ; 
DI, the first, and II, and 
III, the second and third 
dorsal nerves ; the origin of 
the posterior primary branch 
is shown in all the nerves ; 
of these p 2, indicates the 
great occipital from the 
second, and p 3, the smallest 
occipital nerve from the 
third. Cervical plexus : 1, 
anterior primary branch of 
the first cervical nerve and 
loop of union with the second 
nerve ; 2, small occipital 
nerve ; 3, great auricular 
nerve ; 3', superficial cervical 
nerve ; 3 n, communicating 
branches to the descenclcns 
noni from the second and 
third ; 3 s, communicating 
to the spinal accessory from 
the third and fourth nerves ; 
4, supraclavicular nerves ; 
the loops or arches of com- 
munication between the four 
upper cervical nerves, and 
between the fourth and 
fifth, are shown; 4', phrenic 
nerve. Brachial plexus-: V, to VIII', and D\ the five roots of the brachial plexus ; 
5, the rhomboid nerve ; 5', suprascapular ; 5", posterior thoracic ; 6, nerve to the 
subclavius muscle ; 7, 7, inner and outer anterior thoracic nerves ; 8, 8', 8", sub- 
scapular nerves. In the larger nerves proceeding to the shoulder and arm from the 
plexus, those of the anterior divisions are represented of a lighter shade, those belong- 
ing to the posterior division darker ; ec, external cutaneous or musculo- cutaneous ; m y 
median ; u, ulnar ; t'c, internal cutaneous ; w, nerve of Wrisberg ; r, musculo-spiral ; c, 
circumflex ; i,i, intercostal nerves ; i' } lateral branch of the same ; ih, intercosto-humeral 
nerve. 

(From Quain.) 




nerve 



the end of the chapter. In localizing the lesion in the spinal 
palsies, the table should be constantly consulted. 

Individual trunks, as well as the whole plexus, may be attacked 
by disease. It is practically impossible to make a clinical differentia- 



6i6 



THE NON-NEUROXIC DISEASES 



tion between diseases of the trunks of the plexus and the roots out of 
which they are formed. 

Traumatic, toxic and infectious causes are here as usual the source 
of the trouble. The first far outnumber the other two. Dislocations, 
fractures, contusions, blows about the shoulder are especially impor- 
tant as causes. 

Compressing tumors, exostoses, aneurism, arteriosclerotic dilata- 
tions are of the nature of mechanical traumata. An arthritis of the 
joint may set up a neuritis in the neighboring nerves. Tight bandages, 
handcuffs, lying on the arm may produce local trouble in the nerves. 

I will now take up in detail some of the special paralyses of the 
brachial plexus and its branches. 

Erb's Palsy. — This is a combined palsy of the shoulder and arm 
and is due to a lesion of the trunk of the brachial plexus formed by the 
fifth and sixth cervical roots. The muscles that are paralyzed are the 
deltoid, the biceps, the brachialis interims, supinator longus and some- 
times the supinator brevis, infraspinatus and subscapular. It is a fifth 
and sixth cervical root or primary trunk palsy. The central parts and 
upper cords of the plexus are damaged. It is often spoken of as the 
upper arm palsy. Traumata are the chief cause of it, though it has 
been seen as an isolated paralysis in toxic and infectious maladies. The 
position of the arm in which the plexus is made to compress for a long 
time the clavicle may cause it. Thus it occurs as an obstetrical palsy, 
as a result of prolonged narcosis with the arm forcibly elevated out- 
ward and backward. Carrying of heavy burdens on the shoulder has 
produced it. It has been seen to occur bilaterally. The arm hangs 
by the side of the body and the forearm cannot be flexed. 

As an obstetrical palsy Erb's type is slow to recover and when dim 
to injury in adults it is apt to be severe. It has all the characteristics 
of a peripheral palsy, such as the flaccidity of the paralysis, the atrophy. 
the loss of reflex and the reaction of degeneration. 

Klumpke's Palsy. — This is a brachial plexus paralysis due to dis- 
ease of the eighth cervical and first dorsal branches. As it involves the 
triceps, the wrist flexors and pronators, and the flexors and extensors 
of the hand, it is often called the lozcer arm palsy. Elevation of the 
arm can take place and the forearm can be flexed and supinated, but 
extension of the forearm is impossible and the hand is entirely 
paralyzed. 

Tumors, exostoses on the first rib, cervical rib, operative traumata, 
syphilitic meningitis and simple neuritis may cause this lower brachial 
paralysis. A total brachial paralysis may recede and leave this form as 
a residuum. In some cases ulnar sensory disturbances are present and 
even median nerve anaesthesia. If the lesion is close to the cord, involv- 
ing the rami communicantes to the sympathetic nerve, vasomotor and 
oculo pupillary phenomena may be observed. 

The usual treatment and nerve suture apply to these palsies. 

Total Plexus Palsy. — This is usually of traumatic, rarely of 
infectious neuritie origin. It occurs sometimes in obstetrical operations. 
All or parts of the nerves may he involved. Sensory as well as motor 
phenomena are in evidence. As the intercosto-humeral nerve often 



THE NON-NEURONIC DISEASES 617 

innervates the inner side of the upper arm. sensation is sometimes pre- 
served here. Regeneration in these cases takes place, but it is slow 
and prolonged and usually is incomplete, thus leaving some paralysis 
and atrophy. The treatment is based upon general principles and along 
the lines indicated under the head of neuritis. The disease cannot be 
confounded with progressive muscular atrophy, because the sensory 
phenomena and reaction of degeneration are so prominent. Arthritic 
palsy is accompanied by the joint manifestations. 

Obstetrical Palsy. — This form of paralysis is of the brachial 
plexus type. It is due to unusual presentations and the use of the fin- 
ger and instruments in the axilla, directly pressing the nerves or forc- 
ing the shoulder and clavicle upward and backward against them. Vari- 
ous manoeuvres have been the cause of it and even the wrapping of 
the cord around the child's neck has resulted in the palsy. Duchenne 
was the first to describe typical obstetrical palsy. It rarely if ever 
occurs in normal deliveries. 

The whole brachial plexus, or a part of it, may be involved. Usu- 
ally the muscles implicated are the deltoid, biceps, brachial is in tenuis, 
supinator longus and brevis and infraspinatus. The paralysis is of the 
usual peripheral, neuritic type with flaccidity, atrophy, loss of reflex 
and reaction of degeneration. 

Sensory disturbances are prominent, though they are, of course, 
hard to discover in infants. The reflex response is the means that we 
must depend upon to indicate their presence or absence. 

Many of the obstetrical palsies belong to the Erb type previously 
described. 

Rarely the trouble is bilateral, though practically it is a local and 
unilateral palsy. 

The disease usually disappears slowly after many weeks or months. 
Permanent damage of some sort usually remains, though complete re- 
coveries have been seen. If there is no inflammation, early electrical 
treatment along lines already indicated under the head of neuritis should 
be employed and persisted in. 

SPECIAL NERVE PALSIES OF THE UPPER LIMB. 
POSTERIOR OR LONG THORACIC NERVE. 

This is not a common trouble and it occurs mostly in young male 
adults. The nerve may be damaged in the suprascapular region or 
in the axilla. Blows, heavy weights, wounds in the axilla may injure 
the nerve. As a rule strains and over-exertion with the arms raised 
above the head are the most prolific cause of it. Young gymnasts, 
trapeze performers and those who use their arms in this way and swing 
the heavy weight of the body from them are the sufferers. The right 
nerve is mere frequently affected than the left. It has been seen to 
follow infection ( diphtheria, typhoid and influenza), rheumatism and 
the puerperium. Verhaagen thinks it may occur as a hysterical phe- 
nomenon. 

The serratus ma gnus is the muscle that is paralyzed. The arm 
cannot be raised above the horizontal and the shoulder is weakened. 



I 



618 



THE NON-NEURONIC DISEASES 



If the arm is held out horizontally, the lower angle of the scapula stands 
outward from the thoracic wall. If the arm is elevated and carried for- 
ward the scapula swings away from the thoracic wall in such a way 
as to produce a deep groove between the latter and its posterior or 
inner edge, thus giving a wing-like appearance to it. When the arm 
hangs limp beside the body, the lower point of the scapula is a little 
clo<ser to the spinal column than it normally should be. 

Pains occur, but typical sensory disturbances do not accompany 
serratus palsy. 

Prognosis is fair. Course slow. Treatment follows the usual lines. 

CIRCUMFLEX NERVE. 

Circumflex palsy is a common trouble. It is usually due to trauma 
or prolonged pressure from crutches, or the wearing of apparatuses 
for shoulder joint and humeral injuries. Infection, intoxication, with 
lead especially, and cachectic states such as diabetes may all provoke 
a circumflex neuritis. I saw it follow a fracture of the head of the 
humerus. It has followed knife wounds in the axilla. Continued ele- 
vation of the arms in sleep has been reported as a cause of it by Ray- 
mond. 

The muscles supplied by this nerve are the deltoid, teres minor and 
third head of the triceps. It is believed to carry the trophic nerves 
to the shoulder joint. It receives the sensation of the entire upper sur- 
face of the shoulder and down the outer side of the arm as far nearly 
as the middle. When this nerve is paralyzed the arm cannot be abduct- 
ed, much less raised to a horizontal position. Sometimes a little power 
of movement is shown in the deltoid from the supply of its anterior 
portion from the anterior thoracic nerves. Rotation of the arm outward 
is impossible. 

Hypasthesia and ancesthesia occur on top of the shoulder and down 
the outer side of the arm as far as the middle. Changes of a trophic 
nature, with late ankylosis even, may take place in the shoulder joint. 

The fixation of the joint caused by rheumatism or arthritis must be 
distinguished from deltoid paralysis. In the former the scapula moves 
with the humerus ; there is no true paralysis in the muscles ; the sensa- 
tions are not typically disordered ; and there is no reaction of degen- 
eration. 

MUSCULOCUTANEOUS NERVE. 

Rarely has isolated paralysis of this nerve been observed. It has 
occurred after dislocation, extirpation of a tumor and pressure. The 
resulting paralysis was in the flexors of the forearm, excepting the 
supinator longus. There was anesthesia of the external surface of the 
forearm. The paralysis of the biceps and brachialis is particularly con- 
spicuous when the arm is supinated and the supinator longus cannot 
flex the elbow. 

SUPRASCAPULAR NERVE. 

This is very rarely damaged alone. It usually accompanies circum- 
flex paralysis from falls, blows and dislocations of the humerus. The 



THE NON-NEURONIC DISEASES 619 

supra- and infraspinatus muscles are paralyzed ; also the teres minor. 
The arm cannot be rotated outward and extra work is thus thrown on 
the deltoid. This is due to the paralysis of the infraspinatus. When 
the supraspinatus and teres minor are paralyzed, it is only important 
in connection with circumflex paralysis. The supraspinatus rotates the 
shoulder inward. This nerve also supplies the joint. 

MUSCULO-SPIRAL NERVE. WRIST DROP. LEAD PALSY. 
COMPRESSION PARALYSIS. 

In the toxic and infectious polyneuritides this nerve is affected 
along with the others. It is preeminently involved in lead intoxication, 
as has been noted under the head of multiple neuritis. Of all the 
nerves of the extremities it is the nerve most frequently diseased. This 
is because of its particularly exposed position and proximity to bone in 
its course around the upper arm in the musculo-spiral groove of the 
humerus. 

Etiology. — Traumata, especially compression by the head when 
the arm is elevated during sleep in drunkards, is the chief cause of 
the paralysis. Alcoholic, lead and senile cachexia predispose to it. It 
is thus often a toxico-traumatic paralysis. It has occurred in sudden 
and severe muscular action, as in the sudden extension of the arm in 
grasping a support when falling, or in violently throwing a ball. Stabs, 
blows, fractures and other traumata have provoked it. In crutch 
palsy and dislocations it is involved more often with other nerves. It 
is said to have followed over-exertion. It has been observed during 
typhoid fever, rheumatism and the puerperium. Once it occurred in 
the beginning of locomotor ataxia. Arsenic, silver and opium intoxica- 
tion have shown themselves in musculo-spiral palsy. 

As a result of chemical alteration, not puncture or direct injury, it 
has followed the hypodermic injection near it of ether, chloroform, 
alcohol and osmic acid. 

Thus many are the conditions in which this nerve, along with 
others, may be diseased. Trauma and toxaemia, however, are the great 
leading causes and especially so in the isolated types of the trouble. 

Symptoms. — This nerve supplies the extensor muscles and skin of 
the hand and forearm. • It extends and supinates the forearm, extends 
the wrist and fingers and slightly adducts and abducts the latter. When 
it is paralyzed therefore the great prominent symptom is wrist-drop. 
The hand hangs limp at a right angle to the arm when the latter is held 
horizontally. There is a spastic flexion of the hand at the wrist. 
when it is brought out of the position it immediately resumes it again. 
The fingers at the metacarpophalangeal joints are flexed. The thumb 
is pressed inward and opposed to the fingers. The patient is absolutely 
incapable of extending the hand. There is a slight power of extension 
in the first and second phalanges of the fingers on account of the action 
of the intact interossei and lumbricales muscles. Th< third phalanf 
are paralyzed like the wrist. 

If the hand and fingers are rested upon a support, a slight abdui- 






620 



THE NON-NEURON I C DISEASES 



Hon and adduction in the fingers may be observed. Abduction and 
hyperextension of the thumb are lost. 

The arm generally rests in a position of pronation. It cannot be 
supinated. If the forearm is flexed, supination may be accomplished 
by the biceps or by the outward rotation of the upper arm with the 
infraspinatus. 

The paralysis is of the ordinary neuritic, flaccid, atrophic type, with 
absence of the reflexes and electrical reactions. 

Paresthesia conslitute the chief sensory disorders, though these 
are not prominent. In fact, they are usually absent in the cases due to 
compression. Numbness and formication are the chief manifestations. 
Hypcesthesia often occurs ; rarely anesthesia. There may be no anaes- 
thesia even when the nerve is completely severed. 

The sensory phenomena are in the radial distribution. This in- 
cludes the radial half of the back of the hand and thumb, the back of 
the first three fingers, excepting the dorsal surface of the last, or both 
distal phalanges, which areas are innervated by the median nerve, and 
the forearm along a narrow strip upon the radial side innervated by 
the posterior inferior cutaneous nerve. 

There are some slight variations in this clinical picture. For in- 
stance, in a high lesion, as in crutch palsy, the anaesthesia is slight and 
is found chiefly on the front of the arm in the area of distribution of 
the external and internal cutaneous nerves. A considerable variety of 
anaesthetic areas may be observed. In crutch palsy and in dislocation 
paralysis the triceps is involved. Even an isolated paralysis of this 
muscle has been observed. 

In lead paralysis the supinators and sometimes the abductor longus- 
pollicis are spared. Forearm lesions may involve the branches of the 
musculo-spiral in such a way individually or collectively as to give 
quite a variety of clinical presentations. It is rare for the nerves below 
the point where the branches for the supinator are given off to> be com- 
pressed. 

In compression paralysis the electrical reactions are not marked, 
if noticeable at all. In severer lesions, such as wounds, lacerations, 
crushes, the reaction of degeneration is generally well developed. 

Later in the disease the tendon sheaths are swollen and there is 
often hyperostosis of the metacarpal bones. 

Prognosis. — Most cases recover. Mild cases run a few weeks. 
Severe cases last many months or a year or more. The degree of the 
reaction of degeneration will foretell somewhat whether the case will 
be a long or short one. Most compression cases recover in four or six 
weeks ; rarely in a few days. Recently I saw a compression case 
(hanging the arm over the back of a chair) in a rheumatic with 
peripheral neuritis, recover almost completely in three or four days. 
Cases due to knife wounds, punctures and dislocations of the head of 
the humerus are not so promising. They usually exhibit signs of 
severe degeneration and therefore require many months to recover. A 
completely severed nerve offers a bad outlook unless it is immediately 
sutured, and then it requires many months for the restoration of its 
function. Ether paralysis runs several months. 



THE NON-NEURONIC DISEASES 62 1 

Treatment. — The general lines of this have already been laid 
down under the head of Neuritis. Remove and avoid the cause. Nerve 
suturing has accomplished some very encouraging results upon the 
musculo-spiral nerve. In freeing the nerve from a tumor, the danger 
of paralysis must always be thought of. Transplantation has been suc- 
cessfully performed upon this nerve. 

After irritative symptoms have subsided there is no treatment so 
available as that with electricity and massage. Rubber muscles and the 
fixation of the hand in hyper-extension with splints and bandages may 
be necessary in old and severe cases. 

The only medicinal treatment that will be called for will be that to 
combat the underlying intoxication or infection. Salicylates may be 
needed for rheumatism, iodides for saturnism, quinine for malaria. 
Hypodermics of strychnine are at times efficacious. 

MEDIAN NERVE. 

An isolated paralysis of this nerve is very rare and is practically 
always due to trauma. The nerve supplies cutaneous branches to the 
entire palm and to three and a half fingers. It stimulates the pronator 
muscles, the flexors of the carpus and the long flexors of the fingers 
(except the ulnar flexor of the carpus and part of the deep flexor of the 
fingers). The outer set of the short thumb muscles and two lumbricales 
are also excited by it. 

The median is frequently involved with other nerves and it is then 
due to luxations, strangulation, as with tight bandage, fractures of the 
bones of the forearm and callus. Forcible muscular contraction of the 
pronator teres, a severe distortion of the wrist, compression of the 
cervical ribs and embolism of the axillary artery have been charged 
with median palsy. 

The median is usually involved in the craft-palsies, which must 
not be confounded with the occupation neuroses. Milkers, drummers, 
cigar-makers, carpet-beaters, dentists, locksmiths and all those who 
have to use monotonously and for prolonged periods certain muscles of 
the arms. The median and ulnar nerves are the most frequent seat of 
puerperal toxic neuritis. 

Disease of this nerve is revealed in a weakened grip of the hand 
and impairment of flexion and abduction of the thumb and flexion of 
the first and second fingers. There is not much change in the attitude 
of the hand except a slight deviation toward the ulnar side. The 
flexion of the basal phalanges ; s not involved. Pronation of the hand 
is lost. 

Median injuries are usually severe ones with the typical atrophy 
and reaction of degeneration manifestations. 

The sensory symptoms are particularly prominent. They consist 
of pains, hyperesthesia and particularly hypcesthesia in the area of 
distribution of the nerve. The entire area may lx* involved, including 
thus the volar part of the palm as Ear as the fourth metacarpal bone, 
the volar surface of the first three, and the radial side of the fourth 
finger and the dorsal surface of the index and middle fingers. < )c- 






622 



THE NON-NEURONIC DISEASES 



casionally anaesthesia is absent. It has even not been pronounced in- 
complete section of the nerve. Anomalous anastomoses, or rather 
anomalous innervations from the ulnar, have upset both the motor and 
sensory appearances of median disease. 

The trophic and vasomotor symptoms are prominent in disease of 
this nerve. Herpes, pemphigus-vesicles, sluggish ulcers, glossing of 
the skin, falling of the hair o>f the skin, striation of the nails, may be 
expected. The skin is bluish and cool. There is often infiltration of the 
subcutaneous tissue. Sometimes hyperidrosis is especially noticeable. 
Amidrosis may occur. 

The lesion determines the prognosis, and the treatment calls for no 
special comment. 

ULNAR NERVE. 

This nerve is frequently paralyzed, more so than the median. It 
stands second to the musculo-spiral in the frequency of its disease. It 

FIGURE 135. 





Showing Ark a of Anesthesia in Ulnar-Nerve Palsy CBowlby). 

is often affected with other nerves by traumata, such as fractures with 
callus, growths, and luxations. Cuts, bruises, blows all figure in the 
etiology. It is subject to pressure paralysis and it enters into the 
pathology of the professional palsies. It is not often affected in lead 
intoxication. It is an accompaniment of polyneuritis, syphilitic neuritis 
and other infectious troubles. Tumors develop upon the ulnar and it 
has exhibited an ascending form of neuritis. 

The nerve supplies cutaneous filaments to the lower part of the 
forearm to a small extent and the palmar and dorsal aspects of the 
hand in the inner half, to the little finger and to the inner or ulnar side 
of the ring finger. 

The muscles stimulated by it are the ulnar flexor of the carpus. 
the deep flexor of the lingers (its inner half), the short muscles of the 
little finger with the pal maris brevis, the inter ossci of the hand, the in- 
ner two lumbricales, the adductor pollicis and the inner half of the 
flexor brevis pollicis. It also furnishes the nerve supply to the joints 
of the elbow, wrist and hand. 

Tight closure of the hand is impossible, the weakness being of 



THE NON-NEURONIC DISEASES 623 

course in the little and ring ringers. The terminal phalanges of the 
last three ringers cannot be flexed, nor can the thumb be adducted. On 
account of the paralysis of the interossei and lumbricales, the claw 
hand or the main- en- griff e appears. The fingers cannot be abducted or 
adducted. 

Atrophy, loss of reflex and the reaction of degeneration accompany 
this paralysis as in all similar peripheral palsies. 

The sensory symptoms are rarely absent in ulnar disease. There 
are pains, hyperesthesia and anaesthesia, sometimes all existing simul- 
taneously. Hypaesthesia usually occurs on the volar surface of the 
hand to a line which passes through the longitudinal center of the ring 
finger and in a corresponding area on the dorsal surface ; in the little 
finger and over the ulnar half of the ring finger. Sometimes the 
sensory disturbance has been limited entirely to the little finger. 

Trophic, vasomotor and secretory changes, such as are mentioned 
in connection with median nerve palsy, are rather common. 

Pressure palsies recover in a few weeks ; severer ones require 
months and years. 

FIGURE 136. 




Complete " claw-hand" in an old ulnar paralysis (cica- 
trix at A). (After Duchenne ) 

The treatment may involve nerve suture, neurolysis (freeing of the 
nerve from tumors, etc.), electricity, massage and the usual measures 
described at length under the head of neuritis. 

A primary spontaneous neuritis of symmetrical distribution is a 
rare condition, occurring in the ulnar nerves of persons of neuropathic 
constitution and supposed to be due to infection. It is very chronic 
and scarcely ever ends in recovery. It has followed the acute infec- 
tious diseases, particularly typhoid fever. There is at first pain and 
paresthesia in the ulnar distribution. The muscles become weak and 
atrophy and the characteristic claw-hand appears. Anaesthesia de- 
velops also. This is probably a true neuritis in which the degenerative 
side of the process takes precedence because the infection is not virulent 
enough to provoke gross inflammation, but with the aid of the neu- 
ropathic heredity is virulent enough to cause damage in the neurones. 
It is a local, not a true, primary disease, as I have explained at the head 
of this chapter. 

Morgan's Disease, or Analgesic Paralysis with Whitlow. There is 
neuritis of the upper extremities in this disease, but it is a complication 
of syringomyelia, to which the reader is referred for its more detailed 
description. 




624 



THE NON-NEURONIC DISEASES 



DORSAL NERVES. 

There are twelve pairs of dorsal nerves, the first pair entering into 
the formation of the brachial plexus. Except this, and the second and 
twelfth, which send cutaneous offsets respectively to the arm and hip, 
the dorsal nerves are almost entirely distributed to the walls of the 
thorax and abdomen. In certain respiratory troubles and neuralgias 
alone are they of any special clinical interest. 



THE LUMBAR PLEXUS. 

Anatomy. — The lumbar plexus is formed by connections between 
the anterior primary divisions of the four upper lumbar nerves. It is 
in the substance of the psoas muscle. It is joined to the sacral plexus 
by a branch from the fourth lumbar nerve to the fifth. 

From the first nerve spring the ilio-hypogastric and ilio-inguinal 
nerves and a communicating branch to the second nerve. The second 
nerve supplies the greater part of the genito-crural and external cutane- 
ous nerves and also transmits a branch to the third, from which some 
of the fibres of the anterior crural and obturator nerves proceed. There 
are two branches from the third nerve — namely, a large one forming a 
part of the anterior crural nerve, and a smaller forming a part of the 
obturator. The fourth nerve sends forth three branches. Two of these 
complete the obturator and anterior crural nerves, while the third con- 
nects with the fifth nerve and thus becomes a part of the sacral plexus. 

This plexus thus innervates the lower part of the abdominal wall 
and the fore part and inner side of the lower limb. 

Disease of the lumbar or sacral plexus is not as frequent as of the 
brachial plexus. The lumbar plexus has been damaged by neoplasms 
in the abdomen, psoas abscess and vertebral disease. A spontaneous 
crural neuritis has been seen. Very rarely is the obturator nerve alone 
affected, though it has been damaged in parturition. The same is to be 
said of the anterior crural nerve. The gouty diathesis, alcoholic intoxi- 
cation and diabetes mellitus have caused disease sometimes in the 
crural. Sometimes it has been a total bilateral paralysis. Fractures 
have damaged the nerves in a few instances ; but they are well pro- 
tected. 

Symptoms. — Sensory symptoms only occur when the two upper 
lumbar nerves are involved. These involve the abdominal wall. An- 
esthesia or hypccsthesia may appear in the area of distribution of the 
anterior and internal cutaneous femoris and of the saphenus major. 
This includes the anterior and inner surface of the thigh, ihe inner sur- 
face of the leg and the inner border of the foot nearly to the great toe. 
This, of course, represents disease in the two lower lumbar nerves and 
their branches. 

The motor paralysis is seen in the inability of the patient to extend 
the leg and flex the hip. This Is a total paralysis. If it is bilateral the 
gait is markedly disturbed. The pectineus and sartorius do not es- 
pecially cause any trouble. When the palsy is unilateral, the patient has 
to step carefully and not Ilex the knee. 



THE XOX-XLUROXIC DISEASES 



62: 



If the lesion is outside of the pelvis or beyond the point of the 
giving off of the branches to the iliopsoas muscle, the extensor cruris 
quadriceps, the sartorius and the pectineus, the paralysis is not a total 



FIGURE 137. 



dxh 




-Diagrammatic out- 
line OP THE LUMBAR AND 
SACRAL PLEXUSES WITH THK 
PRINCIPAL NERVES AIUSINQ 
FROM THEM. (A. T. ) h 

DXII, the divided roots c. 
the last dorsal nerve ; LI, to V, 
the roots of the five lumbar 
»erves ; the loops uniting the 
-interior primary divisions of 
these nerves together, and the 
first with the twelfth dorsal, arc 
shown ; SI, to V, and CI, the 
sacral and coccygeal nerves ; p, 
placed on some of the nerves 
marks the posterior primary 
divisions cut short ; p, p\ the 
plexus formed by the union of 
the posterior branches of the 
third, fourth, and fifth sacral 
and the coccygeal nerves ; d, 
anterior division of the last 
dorsal nerve, from which d! the 
lateral cutaneous branch arises ; 

I, ilio-hypogastric nerve ; 1', 
ilio-inguinal ; 2, genito-crural ; 
2', external cutaneous of the 
thigh ; ps, branches to the psoas 
muscle ; cr, anterior crural 
nerve; U, branches to the 
iliacus ; ob, obturator nerve ; 
of, accessory obturator ; IV, 
V, loop from the fourth and 
fifth lumbar, forming the lumbo- 
sacral cord ; 3, superior gluteal 
nerve ; sc, great sciatic nerve, 
continued from the sacral 
plexus ; 4, small sciatic nerve, 
rising from the plexus poste- 
riorly ; 4', inferior gluteal nerve ; 
5, inferior pudendal ; 5', poste- 
rior cutaneous of the thigh and 
leg ; 6, 6, branch to the obtu- 
rator internus and gemellus su- 
perior ; 6', 6', branch to the 
gemellus inferior, quadratus 
femoris and hip-joint ; 7, twigs 
to the pyriformis ; 8, pudic 
nerve ; 9, visceral branches ; 9', 
twig to the levator ani ; 10, 
perforating cutaneous nerve ; 

II, coccygeal branches. 



(From Quain.) 



plexus one and hence is incomplete and more limited. In such c 
severe pain is caused in the region supplied l>v the nerve that is irritated. 
This occurs sometimes early and is often due to a neoplasm near the 






626 



THE NON-NEURONIC DISEASES 



spine. The pains follow the course of the crural and saphenus nerves. 
The paralysis is of the ordinary neuritic type with atrophy, reaction 
of degeneration, loss of reflexes and is entirely flaccid. 

OBTURATOR NERVE. 

This nerve rarely suffers alone. It has, however, been so affected 
in tumors and difficult labors. Adduction of the thigh is impossible. 
The patient cannot throw one leg across the other. There is also some 
impairment in both external and internal rotation. There are sensory 
disturbances on the median upper third of the thigh. 



ANTERIOR CRURAL NERVE. 

Here there is weakness in the muscles on the front of the thigh. 
The leg cannot be normally extended. Anaesthesia and pain occur in the 
crural area. 

External Cutaneous Nerve. — Only lately has an isolated paralysis 
of this nerve been noted. There were pains, anaesthesia, parcesthesia 
and other sensory disorders in the area supplied by this nerve. Walk- 
ing and standing seemed to bring on the symptoms. 

Superior Gluteal Nerve. — Gowers mentions that this nerve is very 
rarely diseased in the isolated form. The gluteus medius and minimus 
are paralyzed. There is loss of abduction and circumduction of the 
thigh. 

THE SACRAL PLEXUS. 

Anatomy. — It should be remembered that the anterior divisions of 
the first four sacral nerves make their exit from the spinal canal through 
the anterior sacral foramina, while the fifth passes out between the 
sacrum and coccyx. The first three and a part of the fourth enter into 
the composition of the sacral plexus. The fifth does not form a part of 
the plexus, but ends on the back of the coccyx. That part of the fourth 
that does not enter as a constituent of the plexus supplies branches to 
the viscera and muscles of the pelvis and a connecting branch to the 
fifth nerve. Sometimes the sixth sacral nerve, or anterior branch of 
the coccygeal nerve, in its union by connecting filaments with the fifth 
and fourth sacral nerves, is said to constitute a coccygeal plexus. 

The first three and part of the fourth sacral nerves then form the 
sacral plexus. Without much interlacement these unite to form a large 
upper and a small lower cord or band. The upper represents the union 
of the lumbosacral cord with the first and second and the greater part 
of the third sacral nerves. It is continued into the great sciatic nerve. 
The lower band has a plexiform arrangement and represents the union 
of the smaller part of the third sacral nerve with the plexus portion 
of the fourth. It is prolonged into the pudic nerve. 

The sacral plexus lies on the anterior surface of the pyriformis 
muscle opposite the side of the sacrum. It escapes through the great 
sacro-sciatic foramen and ends at the lower border of the pyriformis. 

In addition to the great sciatic and pudic nerves, it gives off a 



THE NON-NEURONIC DISEASES 627 

number of collateral branches, such as the superior gluteal, which oc- 
cupies an intermediate position between the two plexuses, lumbar and 
sacral, the inferior gluteal, the small sciatic, the perforating cutaneous 
and branches to the pyrifonnis, obturator interims, ge nielli and quad- 
rat us f em or is muscles. 

Diseases of the sacral plexus usually mean the sciatic nerve and its 
branches. Pelvic fractures during parturition, either natural or artifi- 
cial, fractures of the lumbar vertebrae, are a source of disease in this 
nerve. The motor manifestations most commonly implicate the per- 
oneal branch. This is especially the case where the pelvis is contracted 
and the pressure of the head is severe and prolonged. The peraneal 
nerve arises from the lumbar sacral cord mostly, which lies on the in- 
nominate crest and not the pyriform muscle, as the rest of the plexus 
does. Its fibrillar are thought to be especially sensitive and susceptible 
to injury, as shown by its early degeneration in disease and the early 
functionless condition of its muscles after death. Among other causes 
of sacral disease are to be mentioned pelvic tumors, parametritis and 
intrapelvic septic processes, subcutaneous injections of ether, mercury, 
etc., nerve-stretching, fractures and dislocations of the femur. 

SCIATICA. 

This is sometimes called neuralgia ischiadic a or malum cotunnii. 
it is a painful condition of the sciatic nerve and its branches, due in my 
opinion, to neuritis, though many authors regard it as a pure neuralgia. 

As stated by the authorities, there are two forms of sciatica, the 
primary and the secondary. By secondary sciatica is meant pain in 
the sciatic nerve provoked by some extra-neural cause, as for instance 
a tumor pressing upon the nerve. It would be well if we could drop 
the term secondary sciatica in this sense entirely, as the name of a dis- 
ease of the sciatic nerve ; for it represents no more an affection of that 
nerve than would the pain caused by a corn on the foot represent an 
affection of the nerve involved. The very symptom-complex of so- 
called secondary sciatica is different from that of the true or primary 
form. In the former the pain is a referred pain, usually peripheral in 
location, and is not elicited by direct pressure or by the usual manoeu- 
vres which elicit the pain in the latter. 

Strictly speaking, there is only one form of sciatica, disease of 
the nerve itself. This disease, it is sometimes said, may be functional 
<>r organic, and hence true sciatica has been divided into idiopathic 
neuralgia of the nerve, and neuritis. Idiopathic functional sciatic neu- 
ralgia is the term employed to cover all the so-called secondary neural- 
gias and all painful states of the sciatic nerve unaccompanied by any 
known or observable changes in the nerve itself or its central connec- 
tions. Such names as gastralgia. cardialgia. cephalalgia, myalgia, neu- 
ralgia, and a host of others that have become engrafted upon the science 
of medicine, are the contributions of practical medicine ; and while they 
may be very comforting to employ in certain obscure cases, their care- 
less and indiscriminate application to well recognized symptom-groups 
and pathological conditions is an unwarrantable looseness in the use 



628 



THE NON-NEURONIC DISEASES 



of language which awakens a suspicion of ignorance or of indolence. 
Idiopathic neuralgia and simple neuritis are constantly being con- 
founded. Though many cases of so-called neuralgia are clearly in- 
stances of neuritis, it is much more convenient in the hurry of gen- 
eral practice to call cases of painful nerves by the undeniable but 
meaningless name of neuralgia than it is to study the electrical reac- 
tions and other symptoms characteristic of neuritis. Dana found, after 
a close study of the subject, that true idiopathic neuralgia is a rare 
disease, constituting not more than two or three per cent, of all the 
different forms of nervous disorders. Symptomatic and reflex neu- 
ralgias are of course far more common. These statistics confirm those 
of Classin, of Kiel, who collected 434 cases. 

On account of the generally favorable termination of sciatica, the 
opportunity for the direct examination of the diseased nerve rarely 
presents itself. In those cases in which it has been examined, how- 
ever, the findings have almost invariably been those of a neuritis or 
perineuritis ; redness with swelling of the nerve-sheath, small hemor- 
rhages in recent cases, spindle-shaped intumescence, dilated arteries, 
serous transudations, migration of the leucocytes, proliferation of the 
connective tissue, adhesions and secondary damage to the nerve-fibres. 
In so great a majority of the cases have these signs of inflammation 
been seen that one is easily justified in suspecting that all cases of pri- 
mary sciatica are cases of sciatic neuritis. This suspicion is moreover 
confirmed by a careful consideration of the etiology, symptoms, and 
therapeutics of sciatica. Among the considerable number of cases 
that have come under my observation, I do not recall one in which I 
was not satisfied that the nerve itself was more or less inflamed. 

Etiology. — The etiology of sciatica, as given in the text-books, 
is remarkably like that of simple neuritis. In one of the recent works 
sciatica is said to be the result of traumatism, exposure, gout, rheuma- 
tism, syphilis, or malaria. Lawson declares that nine-tenths of the 
cases of sciatica are due to exposure to cold, while Erb insists upon 
the preeminence of this above all other causes. Many authors, as, for 
instance, Gowers, Tyson, Osier, Anstie, and Weir Mitchell, speak of 
syphilis as an infrequent cause of sciatica. They doubtless refer to 
sciatic neuritis; for just like intracranial syphilis, which so frequently 
affects the nerves of the ocular muscles without causing any inflam- 
mation in these nerves, so syphilis may cause a secondary sciatica or 
pain in the nerve by a neoplastic pressure, without giving rise to a 
primary sciatic neuritis except in rare cases. Infectious diseases, such 
as typhoid fever, variola, diphtheria, tuberculosis, intoxicants such as 
alcohol and nicotine, diabetes, and other toxaemic conditions, may all 
predispose to an attack of sciatica, as well as to a general neuritis ; 
but exposure to cold and damp, and direct injury of the nerve, are the 
chief factors that start the attack. Among the traumatic causes may 
be mentioned contusions and wounds in the perineum, buttocks, pelvis, 
by falls, pressure, slow, difficult parturition and hard fecal masses. 
Perimetritis may cause it. The character and location of these causes 
will determine the unilaterality or bilaterality of the sciatica. 

It is a noteworthy fact, when considered in this connection, that 



THE NON-NEURONIC DISEASES 629 

heredity and predisposition are of less importance in the etiology of 
sciatica than they are in the neuralgia of other nerves. 

In persons suffering from varicose veins, Quenu found the veins 
in the interior of the sciatic nerves greatly dilated. Of sixty-seven 
individuals with varicose veins eleven were the victims of sciatica. 

A case of my own was a German woman, fifty-two years of age, 
with varicose veins of the right leg, who suffered at rare intervals with 
slight attacks of pain along the course of the corresponding sciatic 
nerve. An elastic stocking and the internal administration of hamame- 
lis afforded her prompt and marked relief. 

Men are more frequently afflicted w T ith sciatica than women, 
though this is probably due to the difference between the sexes in re- 
gard to the incidence of the many other causes of the disease. This is 
shown by the fact that it is a disease of middle life, being rare in ex- 
treme old age and practically unknown in childhood. 

Pathology and Pathogenesis. — This is the same as any form 
of peripheral neuritis. It is true that in some cases there are no find- 
ings. It is probable that in such cases the changes have been very 
slight and evanescent, or the central representation of the nerve may 
have been functionally at fault. These constitute a small minority of 
cases and I am of the opinion that if in every case we could examine 
microscopically the entire nerve we would find more often than we 
now do positive signs of neuritis. 

Symptoms. — These begin gradually and steadily increase to a cli- 
max in the course of a few days or weeks. It is oftener the rule than 
the exception for the inflammatory process in neuritis to be more in- 
tense at particular points in the course of the nerve. Indeed, a large 
number of these cases might well be called focal neuritis, on account 
of the higher degree of the inflammation at these points or foci. The 
pain is usually sharper there on account of the greater damage and 
severer pressure upon the nervi nervorum. And yet what are these 
tender points of neuritis but the classical puncta dolorosa of neuralgia! 
These puncta are described as being usually situated in the neighbor- 
hood of bony prominences. Yalleix, who was the first to draw atten- 
tion to them, said they would be found to correspond with the poste- 
rior superior spine of the ilium, the spine of the ischium where the 
nerve makes its escape from the pelvic cavity, the great trochanter of 
the femur behind which the nerve runs near the border of the gluteus 
maximus, the head of the fibula, the internal malleolus, and the dorsum 
of the foot. 

In sciatic neuritis it is easy enough to explain the tenderness of 
the nerve-trunk by means of the inflammatory irritation and pressure 
upon the nervi nervorum; but in so-called idiopathic neuralgia, in 
which there is supposed to be no perceptible lesion of the nerve-trunk, 
it is difficult to comprehend how such exquisite local pain is to be 
accounted for. Idiopathic neuralgic pain is not localized in the nerve- 
trunk, but rather in the peripheral distribution of the nerve and its 
branches. At all events it would not be so keen in the nerve-trunk as 
it is in neuritis. Every one knows, however, that the local pain in 



630 



THE NON-NEURONIC DISEASES 



sciatica is usually so severe that the patient dreads to be touched, and 
finds sitting down often a most distressing act. 

Pathology has not yet discovered any change in the trunk of a nerve 
attacked with so-called idiopathic neuralgia. The change, whatever it 
may be, is either at the peripheral or central end of the nerve. There are 
no sensory cells in the course of the nerve itself or its constituent 
fibers whereby painful impressions are received and transmitted to the 
brain. And yet neuralgia is one of the most painful of all affections, 
and the pain, as in sciatica, is even more intolerable in the nerve-trunk 
than it is at the periphery. Those who deny the inflammatory char- 
acter of these painful sciaticas have no easy task before them to ex- 
plain the immediate cause of the pain. In opposition to all the teach- 
ings of physiology, they must show how a relatively inert nerve-fiber, 
capable merely of transmitting different impulses, can, when unaf- 
fected by any perceptible pressure or irritation within or outside of 
its own substance, give rise to the most excruciating agony. To say 
that this pain is functional in character, and therefore does not nee 'I 
any perceptible change in the nerve structure to account for it, only 
enhances the difficulty, for functional pains are always referred to 
the extremity of the nerve and its branches and never directly to the 
nerve-trunk. And again, to say that the nervi nervorum found in the 
course of the nerve-trunk are the peripheral sources of this so-called 
idiopathic neuralgia as functional pain, needs a further explanation as to 
how these nervi nervorum come to be the sources of this pain in the 
absence of any pressure or damage to them. Does it not seem singu- 
lar that this mysterious, imperceptible agent of idiopathic neuralgia 
can thus arouse to the highest degree the function of a sensory nerve 
and yet not at the same time affect the motor strands? The motor 
nerves along the course of their trunks are like the sensory nerves ; 
yet motor spasm, pure and simple, is not a symptom of idiopathic 
neuralgia. 

In typical neuritis there are associated with the pain along the 
course of the nerve-trunk peculiar sensations, paresthesia, and various 
degrees of motor paresis in the parts supplied by the nerve and its 
branches. In fact, the combination of pain in the course of the nerve- 
trunk with various spontaneous irritative motor and sensory phenomena 
at its distal extremity, is almost pathognomonic of an inflammation of 
the nerve. The pressure and irritation of the nervi nervorum and re- 
current fibers sufficiently explain the former, while interference with 
the power of conduction by the same pressure readily accounts for 
the latter. And yet some of the authorities still assert that in simple 
neuralgia of the sciatic nerve there occur various paresthesia?, tonic 
and clonic spasms in the leg, and even at times a considerable degree 
of paralysis. In other words, when the nerve is apparently quite un- 
changed histologically, it is affected functionally in such a mysterious 
way as to give rise to a paralysis and symptoms of irritation at the 
same time. The argument itself is a reductio ad absurd inn. The 
nerve, it is maintained, is so sensitive that the condition is deemed 
worthy of the dignity of a special name, neuralgia ; while at the same 
time the nerve is so dead in function as to fail in the proper conduc- 



THE X0X-XEUR0X1C DISEASES 63 I 

tion of received impressions. Usually, irritation is the cause of mus- 
cular spasm ; here, however, irritation is made more frequently to ac- 
company paralysis. There is a conflict here between physiology and 
pathology which those who insist upon the non-inflammatory char- 
acter of idiopathic sciatica will do well to explain. 

The pain of sciatica is a localized pain, rarely diffuse, and is bor- 
ing, tearing, and burning in character. It is often so localized that 
the patient can almost feel the entire nerve like a cord passing down 
the back of his leg. Like all inflammatory pains, it varies in intensity 
and is increased by movement and pressure. Walking, straining, 
coughing, prolonged sitting increase it. It may be excited by the 
finger in the rectum or vagina. Placing the patient on his back and 
attempting extreme flexion of the legs, on the body is an excellent 
diagnostic manoeuvre, as it often cannot be done on account of the ex- 
treme pain produced. Sometimes the skin is red and slightly oedema- 
tous, and the local temperature may be somewhat elevated. The earli- 
est indications of involvement of the nerve-fibers are the peripheral 
par&sthesia and hyperesthesia for the sensory, and fibrillary twitch- 
ings and tonic contractions of the muscles for the motor. The reflexes 
are somewhat increased at first, but diminished in old cases. The 
electric excitability is at first enhanced, and then more or less lost. 
In subacute and chronic cases there will be some reaction of degenera- 
tion. Trophic disturbances sometimes observed include muscular 
atrophy, herpes, excessive perspiration, and even joint affections. 

In simple neuritis, posture is at times almost as pathognomonic as 
is pain upon movement. See illustration where the patient shows in 
her comparative attitude, the painful and weakened condition of the 
left leg. The faulty attitude of the body, so characteristic in sciatica, 
is an old and well recognized symptom. Sometimes the patient leans 
toward the painful side, sometimes away from it ; but always in a 
direction to modify the severity of the pain. By the manoeuver the 
nerve is probably lifted away from certain prominences in the pelvis 
against which it usually rests. When there is scoliosis of the lumbar 
column, the concavity is usually towards the sound side. Various ex- 
planations of this have been given, none of which are entirely satis- 
factory. Many think it is due to the effort to relieve pressure on the 
sensory nerve and its branches ; others think it is due to a muscular 
weakness: still others hold that it is dependent upon the muscular 
spasm and contracture. Occasionally kyphosis may be seen. 

Neuralgia of other nerves generally occurs under verv different 
conditions from those under which neuralgia of the sciatic usually 
takes place. The victims of such neuralgias often suffer from migraine. 
pains in some of the special nerves of the head and of the viscera, which 
pains are remarkably disposed to become periodic. Headaches an 1 
visceral pains are quite infrequent among patients suffering from pri- 
mary simple sciatica. 

DIAGNOSIS. — Sciatica is more often diagnosed in practice than it 
actually occurs. Either from the obscurity of the • the lack o\ 

care in the examination, various lesions of the pelvis, the hip-joint, the 



632 



THE NON-NEURONIC DISEASES 



spine and elsewhere, involving the sciatic nerve and causing it to be 
painful, pass under the name of sciatica. 

No disease demands a more earnest effort at differential diagno- 
sis. Its clinical picture is characteristic enough and there is no ex- 



FIGURE 138. 



FIGURE 139. 





Subacute sciatic neuritis. Dr. Fitch's case. The left side is the arfected 
one, as shown by the difference in the attitude, when resting upon one or the 
other leg. 

cuse, except in the rarest instances, for sonic of the gross blunders 
that are sometimes made. The onset and location of the pain, its 
variation under certain characteristic manceuvers ; the puncta dolorosa 
and general tenderness along the course of the nerve, the bodily atti- 



THE NON-NEURONIC DISEASES 633 

tude and disorders of motility, the etiology and course of the entire 
affection are distinctive. 

As I am convinced that all forms of genuine peripheral sciatica 
are neuritic in nature, it is unnecessary to attempt a differential diag- 
nosis between what is called sciatic neuralgia and sciatic neuritis. The 
sensory phenomena, the atrophy, the reaction of degeneration, the 
altered reflexes are the same in both but differ very widely in degree 
in different cases. In some instances they appear only slightly and 
then not until late in the disease. These are the chronic cases. 

Coxalgia from tuberculosis or other disease of the hip- joint is 
characterized by the peculiar attitude of the leg and the referred pains 
in the knee-joint. The sciatic signs are wanting. 

Hysteria, hysterical sciatica, hemorrhoids, arteriosclerosis, arteritis 
obliterans, varicose veins, various vasomotor spasmodic conditions, 
need but to be mentioned as causes of pains in the legs that may simu- 
late sciatic neuritis. None but a tyro in medicine, or one who is 
superficial in his examinations, would mistake these conditions with 
their distinctive subjective and objective exhibitions for a true dis- 
ease of the sciatic nerve. 

A bursitis, following gonorrhoea, malaria or trauma may cause 
an achillodynia, or pain at the insertion of the tendo Achilles, upon 
walking and standing. 

Inflammation of the calf-muscles, a myositis, may be the cause of 
the pain in some cases. The other distinctive signs and history of 
sciatica will be absent. 

The gouty diathesis, faulty footwear, excessive use of the feet 
in standing, neurasthenia, may provoke pain in and about the fourth 
metatarso-phalangeal articulation. This is Morton's metatarsal gia and 
is usually relieved when the cause is discovered. 

Prognosis. — The underlying diathesis and predisposition may de- 
termine the course and prognosis of sciatica. Acute cases due to 
acute causes usually get well in a few weeks. Chronic cases sometimes 
run their course with more or less periodic exacerbations. Remissions 
and even intermissions occur. Rheumatic cases are usually favorable. 
Very old cases, senile cases and those due to unchangeable causes can- 
not hope for more than occasional amelioration, with or without treat- 
ment. Permanent lameness occurs in some. 

Treatment. — In the management of sciatica the methods that 
afford the highest degree of success are not only different from those 
employed in the treatment of other neuralgias, but they are more or 
less identical with those that prove to be most efficacious in the man- 
agement of neuritis. Counter-irritation and the actual cautery even, 
the internal administration of vasomotor sedatives, the free use of 
cathartics, diuretics, and diaphoretics, are the chief measures depended 
upon in the subacute and acute stage. Analgesics, narcotics, and sen- 
sory depressants produce less permanent results in sciatica than they 
do in other forms of neuralgia, doubtless because they do not affect 
the organic changes underlying the trouble. 

According to Pliny, the victims of sciatica in his day had their 
pains assuaged by the soft tones of the flute. From this ancient musical 



634 



THE NON-NEURON IC DISEASES 



method to the modern hypnotic it is not such a far leap. Pain may 
become a habit even after the organic cause of the pain has disap- 
peared, a habit which often needs only moral and mental treatment for 
its relief. In such cases, and they are usually long-standing ones, 
electricity, baths, moderate exercise, and general hygienic treatment 
will do much. Most of these cases were undoubtedly neuralgias. 

Drugs are useful, though secondary in the treatment of sciatica. 
In the acute stage, general and absolute rest, even to the point of strap- 
ping the limb if necessary, is a sine qua non. To paralyze the sensi- 
bility and depress the excited circulation, opium and its alkaloids, acon- 
ite, belladonna, antipyrin, phenacetin, acetanilid, are all most useful. 
So many cases are associated with the rheumatic and gouty diatheses 
that I find myself making large use of the salicylates and colchicum, and 
with general good results. The deep injection of ether and 
chloroform, though useful sometimes, has not proved uniformly so in 
my hands. In old cases, nerve-stretching may be done surgically, or 
less radically by placing the patient on his back and flexing the legs 
on the body as far as possible. Sometimes this has broken up a long- 
standing sciatica, possibly doing it by breaking up small, old adhesions 
and restoring the circulation. 

After the trouble has become chronic and all acute signs of in- 
flammation have disappeared, I resort to the steady use of strychnine, 
preferably by the subcutaneous method as recommended by Leyden, 
in doses of from 1-70 to 1-20 of a grain twice a day. Massage, baths, 
and the steady use of mild currents of electricity should be made every 
day. For the general principles of treatment see the section on neuritis. 

Peroneal or External Popliteal Nerve. — It is a curious fact that 
in all sciatic diseases, the symptoms of the peroneal are more prominent 
than of other branches. As an isolated paralysis the peroneal is far 
more frequently affected than the tibialis posticus. In my own opinion 
there is a developmental, biological reason behind this, though as yet 
we cannot determine just what it is. It is one of the curious facts of 
nature that goes with such exhibitions as the localization of syphilitic 
damage in special neurones in tabes, and the causation of a thyroid-like 
disease, acromegaly, out of a hypophyseal lesion. Note the frequency 
of its disease in acute anterior poliomyelitis in this connection. 

The nerve may be injured by fracture of the fibula and callus. 
by lacerations in running and making missteps, and by forcible exten- 
sion of the leg. It has been badly compressed by a tourniquet, by 
sleeping cross-legged, by wearing of stilts and by prolonged stooping 
in certain occupations, like potato-picking. 

The nerve supplies the tibialis anticus, the long extensor of the 
toes, the short extensor and the peronei. Consequently, the foot drops; 
it cannot be flexed at the ankle. Ultimately talipes equinus develops. 
The first phalanges of the toes cannot be extended. The unopposed 
interossei cause persistent flexion of the first phalanges. This leads 
to the pied-en- griife appearance. Walking, of course, is difficult and 
the toes drag on and scrape the floor. The dorsum of the foot and 
outer half of the leg is apt to be ancesthetic. 

The paralysis is of the degenerative type with atrophy, loss of re- 



THE N0N -NEURONIC DISEASES 635 

flexes, reaction of degeneration. It is therefore flaccid. Anomalies 
occur in both the motor and sensory phenomena. Thus the tibialis 
amicus may escape the palsy and the anaesthesia may not limit itself 
strictly to the peroneal area. 

Trophic and vasomotor symptoms occur. 

Tibialis Posticus, or Internal Pop! ileal. Here the popliteus, calf 
muscles, tibialis posticus and long flexors of the toes are involved. The 
plantar muscles are implicated. The ankle joint cannot be extended 
and the flexed leg cannot be rotated inward. Talipes calcaneus is the 
deformity that ultimately results. The patient cannot raise himself on 
his toes. The sole of the foot and the lower haif of the outer part of 
the back of the leg is anesthetic. 

Plantar Nerves. — These rarely are diseased alone. Disease of the 
internal causes anaesthesia on the inner part of the sole and the plantar 
surface of the three inner toes and half of the fourth. The short flexor 
■of the toes is paralyzed, the plantar muscles of the great toe except 
the adductor and the two inner lumbricales. Disease of the external 
reveals itself in anaesthesia in the outer half of the sole, the little toe 
and outer half of the fourth ; paralysis of the flexor accessorius, of 
the muscles of the little toe, all the interossei, the two outer lumbricales 
and the adductor of the hallux. As the toes gradually become flexed 
persistently at the last two joints, and extended at the others, walking 
is badly interfered with and the appearance is that of the pied-en- 
griffe. 

The prognosis and treatment of all of these neuritic troubles of 
the lower limbs follow the same line that they do in the similar troubles 
in the upper limb. For the general principles, the reader is referred to 
the section headed neuritis. 









6 3 6 



THE NON-NEURONIC DISEASES 



The following table is taken from Dana's work and is a compilation from 
Starr, Mills, Sachs, Thorburn, Dana himself and others. 



Muscles of Tongue, Palate, and Pharynx. 













Diseases in 


Name of 


Normal 


Symptoms of Defi- 


Innervated 


Represented 


which Muscle is 


Muscle. 


Function. 


cient Action. 


by 


in 


commonly In- 
volved. 


Genio- 


Pushes tongue 


Tongue when pro- 


The twelfth 


Medulla. 


t 


glossus. 


to opposite 


truded deviates to 


nerve (hy- 








side. 


paralyzed side. 


poglossal). 






S t yloglos- 


Raises tongue 


Tongue cannot be 


The twelfth 


Medulla. 


Bulbar pal- 


.sus. 


backward and 


moved backward 


nerve. 




sies (acute 




upward. 


or hollowed out 
(action deficient 
in many healthy 
subjects). 






and chron- 
ic) ; in spe- 
cific and tu- 
• b e r c ulous. 


L i ngual 


All movements 


When lying in 


The twelfth 


Medulla. 


diseases o f 


muscle 


of the tongue 


mouth deviation 


nerve. 




base ; dys- 


proper. 


itself. 


to healthy side ; 
when protruded 
deviates to para- 
lyzed side; if one 






troph ies. 
(rare). 
















or both halves are 












atrophied tongue 












looks shrivelled. 








A zy go s 


Shortening of 


Uvula deviates to- 


Probably Medulla. 


As above. 


uvulae 


uvula. 


ward sound side ; 
if both sides are 
paralyzed there 
are nasal tone 
and regurgitation 
through nose 


pharyngeal 
plexus; 
seventh 
nerve (?). 






Name of 


Normal 


Symptoms of Defi- 


Innervated 


Represented 


Diseases in 
which Muscle is 


Muscle. 


Function. 


cient Action. 


by 


in 


commonly In- 
volved. 


Levator 


Raises the ve- 


Arch cannot b e 


As above. 


Medulla. 


As above ; see 


palati. 


lum palati. 


raised in the in- 
tonation of 4t ah;" 
if paralysis is bi- 
lateral flapping of 
arch and regurgi- 
tation of food 






also seventh- 
nerve affec- 
tions. 
















through nose. 








Palato- 


Prevent food 


Regurgitation o f 


The fi f t h ]P 


Basilar affec- 


pharyn- 


from passing 


food ; nasal 


nerve 




tions. 


geal mus- 


toward up- 


speech. 








cles. 


per part of 
pharynx and 
post er i o r 












nares. 








Stylo- pha- 


Helps to draw 


Imperfect degluti- 


Glosso - pha- 


Medulla. Bulbar affec- 


ryngeus. 


larynx up- 


tion ; food gets 


ryngeal. 




tions and dis- 




ward so as to 


into windpipe. 






eases of the 




be closed by 








base. 




epiglottis and 












overtopped 












by tongue. 










Cons tric- 


Help to push 


Food is swallowed 


P h a ryngeal 


Medulla 


Diseases of the 


tors of 


food into gul- 


very imperfectly ; 


plexus. 




base (bulbar). 


pharynx. 


let. 


sticks in throat. 








Laryngeal 
muscles. 


Movements of 


Hoarseness and 


Recurrent 


Medulla 


B ul bar trou- 


vocal cords in 


difficulty in 


la ryngeal 




bles (similar 




respiration 


breathing; laryn- 


nerve ex- 




symptoms 




and in articu- 


goscopy examina- 


cepting the 




may be caused 




lation. 


tion reveals false 


crico - 1 h y- 




by tumors and 






position of vocal 


roid m u s- 




foreign bodies 






cords (see special 


cle. 




in larynx). 






text-books) 









THE NON-NEURON F<: DISEASES 



r W 



Muscles of Head and Neck. 











| 


Diseases in 


Name of 


Normal 


Symptoms of Defi- 


Innervated 


Represented 


which Muscle is 


Muscle. 


Function. 


cient Action. 


by 


» 


commonly In- 
volved. 


Sterno- 


Raises and 


Inability to raise 


1 
Spinal ac- 


Medulla and 


In bulbar and 


cleido- 


turns face to 


head from bed. or 


cessory. 


second and 


cervical - co r d 


mastoid. 


opposite side; 


other horizoutal 




third cer- 


affections ; in 




head inclines 


position, if both 




vical seg- 


later stages of 




to same side; 


muscles are affect- 




ments. 


progressive 




if both mus- 


ed; if one muscle 






muscular 




cles act Con- 


is affected, no 






atrophies; 




jointly head 


marked change of 






occasionally 




is brought 


position, unless 






in neuritis. 




forward.' 


opposite muscle 
is contractured ; 
spasm of muscle 
frequent; head in- 
clined to one side. 








"Rectus 


To flex head. 


Cannot flex bead ' 


L 

i Upper cervi- 

I cal. 


Upper c e r- 




capitis 




so as to bring 


vical seg- 




a n t icus 




chin on chest. 




ments, 




major. 












Rectus 


To flex head. 










capitis 












amicus 












minor. 










Diseases o f 
the cervical 


Rectus 


Slight rota- 


Deficient rota- 






region (niy- 


capitis 


tion. 


tion scarcely 






■ elitis, men- 


lateralis. 




noticeable, un- 
less sterno-clei- 






i n g i t i s , 
tumor; pro- 
gressive 






do-mastoids are 










diseased. 






wasting o f 


Scaleni 


Elevate ribs- 


Deficient inspi- 


Lower cervi- 


Lower cervi- 


muscles) 


anterior 


when verte- 


ratory m o v e- 


cal nerves. 


c a 1 seg- 




medi- 


bral column 


ments. 




ments. 




u s, e t 


is fixed ; aid 










poste- 


in inspira- 










rior. 


tion ; slight 
lateral flex- 
ion. 












Flexion of ver- 


Imperfect flexion 


Lower cervi- 






Lon gus 


tebral col- 


of upper spine. J 


l cal nerves. 




J 


colli. 


umn. 











638 



THE NON-NEURONIC DISEASES 



Muscles of Shoulders and Upper Extremity. 



Name of 
Muscle. 



T rapezius 
1. Cla- 
vicular 
portion 
(respi- 
ratory; 
o-u t e r 
third of 
c 1 a v i c le 
to occipi- 
tal bone) 



2.Middle 
portion 
(from 
acromion 
and outer 
spine o f 
scapula to 
ligament. 
n u c h m 
and up- 
per dorsal 
spines v. 

3. Lower 
portion 
and ad- 
ductor 



R h o m 

boids. 



Normal 
Function. 



Levator 
a n g ul i 
scapulae. 



Serratus 
magnus. 






Pulls head 
backward; ro- 
tates slightly 
toward side of 
muscle, so 
that chin is 
turned to op- 
posite side; 
contraction of 
both clavicu- 
lar portions 
bends head 
backward ; 
slight eleva- 
tion of shoul- 
ders; aids in 
deep inspira- 
tion. 

Raises shoul- 
der-blad e ; 
elevation o f 
acromion 
(clavicle goes 
along). 



Adduction o f 
scapula to- 
ward median 
line. 



Oblique move- 
ment of scap- 
ula from be- 
low, upward 
and inward, 
so that infe- 
rior angle is 
brought near- 
er the medi- 
an line; hold 
spinal margin 
of scapula 
down to tho- 
rax. 



Draws superi- 
or inner angle 
of scapula up- 
ward; aids 
in shrugging 
of shoulders. 

Rotation of 
shoulder- 
blade out- 
ward, and 
slight eleva- 
tion of acro- 
mion; holds 
inner margin 
of scapula to 
thorax ;brings 
arm from hor- 
izontal to ver- 
tical position. 



Symptoms of Defi- 
cient Action. 



Innervated 
by 



Deficient back- 
ward movement 
of head; not 
maiked as a rule 
because deep 
muscles perform 
this function ; 
shoulder does not 
move during in- 
spiration. 



Acromion depress- 
ed by weight of 
upper extremity ; 
inner upper an- 
gle may be pulled 
upward by levator 
anguli scapulae; 
internal lower an- 
gle is nearer to 
median line. 



Margin of scapula 
is about ten cm. 
distant, instead of 
being five or six 
cm. distant from 
median line ; loss 
of adductor may 
be covered up by 
action o f rhom- 
boids ; rounding 
of back. 

Deep groove be- 
tween inner mar- 
gin of scapula and 
thorax; if serra- 
tus is normal, this 
groove disap- 
pears if arm is ex- 
tended forward ; 
shoulder blade 
cannot be approx 
iinated to median 
line. (According 
to Duchenue this 
can be effected by 
upper portion of 
latissimus dorsi.) 

Isolated paralysis 
rare. 



Scapula pulle<.r\ip- 
ward; lower inner 
angle nearer the 
median line; arm 
cannot be raised 
above horizontal 
position; if arm is 
stretched forward 
scapula is re- 
moved from tho- 
rax (''winged 
scapula 1 '); dur- 
ing abduction of 
arm, scapula i? 
moved nearer to 
median line, and 
crowds trapezius 
and rhomboids 
forward. 



Spinal acces- 
sory 



Spinal acces- 
sory nerve. 



Represented 



Medulla and 
second and 
third cervi- 
c al seg- 
ments. 



As above. 



Diseases in 
which Muscle is^ 
commonly In- 
volved. 



Progressive- 
m u sc u 1 a r 
wasting ; dis- 
eases of me- 
dulla and up- 
per cervical 
cord ; clavic- 
ular portion 
least frequent- 
ly involved. 



As above. 



Spinal acces- 
sory nerve. 



Fifth cervi- 
cal. 



Third and 
fifth cervi- 
cal nerves. 



Posterior 
thoracic 
nerve. 



Medulla and 
second and 
third cervi- 
c a 1 seg- 
ments. 



Fourth and 
fifth cervi- 
cal seg- 
ments. 



Second and 
fourth (?) 
cervical 
segments. 



Fifth and 
sixth cervi- 
c a 1 seg- 
ments. 



As above. 



Dystrophies 
and cervical 



Progressive 
muscular atro- 
phies ( d y s- 
trophies); neu- 
ritis of part of 
the brachial 
plexus ; after 
traumatic in- 
juries to shoul- 
der : in cervi- 
cal-cord affec- 
tions. 



THE XOX-XEUROXTC DISEASES 



639 



Muscles of Shoulders and Upper Extremity. — Continued. 



Name of 
Muscle. 



Deltoid 
(three di- 
visions). 



lufraspi-") 
natus. ! 

Teres f 
minor, j 

Subscap- 
u'aris. 



Supras p 1 
natus. 



Latissimus 
dorsi. 



Teres ma- 
jor. 



Pectoral is 
major. 



Normal 
Function. 



To raise arm 
to horizontal 
position, and 
forward, out- 
ward, or back- 
ward ; move- 
ments possi- 
ble only i f 
scapula is 
fixed by ac- 
tion of serra- 
tus and tra- 
pezius. 

Rotator hu- 
meri posticus 
( Duchenne ) ; 
rotate arm 
outward. 

Rotator hume- 
ri a n/t i c u s 
(Duchenne) ; 
rotates arm 
inward 

Helps to 
steady shoul- 
der-joint and 
to elevate 
arm forward 
and outward ; 
outer antdeof 
scapula is de- 
pressed. 

Pulls the arm 
when raised, 
downward 
and back- 
ward; if arm 
is at rest up- 
p e r portion 
brings scap- 
ula nearer 
the median 
line ; united 
action of up- 
per third of 
both muscles 
causes exten- 
sion of dorsal 
trunk ; single 
action causes 
lateral move- 
mentof trunk. 

Rotates raised 
humerus in- 
ward; adduc- 
tion of arm to 
thorax; slight 
elevation o f 
shoulder. 

Clavicular 
portion d e - 
presses hu- 
merus from 
raised posi- 
tion to hori- 
zontal ; ad- 
duction of 
arm, as in 
giving a hless- 
ing: sternal 
portion de- 
presses arm 
com pletely, 
and if arm is 
at rest draws 
acromion for- 
wsrd and 
backward. 



Symptoms of Defi- 
cient Action. 



Innervated 
by 



Represented 



Can raise shoulder 
but not arm; 
shoulder flattened 
(atrophy) ; groove 
between acromion 
and head of hu- 
merus ; each di- 
vision of deltoid 
may be paralyzed 
singly. 



Arm cannot be 
moved outward. 

Difficulty in writ- 
ing (Duchenne). 

Arm cannot be 
moved inward ; 
scapula is rubbed 
against ribs. 

According to Du- 
chenne, humerus 
is separated still 
farther from acro- 
mion, if supra- 
spinatus is affect- 
ed in addition to 
deltoid. 

Arm cannot b e 
moved backward : 
insufficient exten- 
sion of dorsal 
spine; trunk can- 
not be moved lat- 
erally. 



Circumflex. 



Very few symp- 
toms; action sup- 
plied b y other 
muscles. 



Imperfect adduc- 
tion of arm ; pa- 
ralysis can be dis- 
covered best by 
extending arms 
and trying to 
press volar sur- 
faces against 
each other. 



Suprascapu- Fourth cer- As above, 
lar vical. 



Supra-] 
scapular. | 

Circum- 
flex. 

Subscapu- 
lar nerve. 



Fourth, fifth, 
and sixth 
cervical 
segments. 



Diseases in 
which Muscle is 
commonly In- 
volved. 



As above ; also 
in Erb's form 
of obstetrical 
paralysis. 



Fourth, fifth, 
and sixth 
ce r v i c a 1 
segments. 



As in case of 
deltoid. 



Subscapu- 
lar, also 
branches of 
dorsal and 
1 u m b a r I 
nerves pass- 
ing through 
muscle. 



Sixth and As in progres- 



seventh cer- 
vical. 



Subscapular. 



Anterior 
thoracic. 



sive atrophies 
and dystro- 
phies; in cer- 
vico- dorsal 
lesions; in 
neuritis. 



Seventh cer- 
vical. 



Fifth, sixth, 
aud seventh 
cervical. 



As above. 



Amyotrophies 
and dystro- 
phies, chiefly; 
also in lesions 
of brachial 
plexus. 



640 



THE NON-NEURON I C DISEASES 

Muscles of Arm, Forearm, and Hand. 













Diseases in 


Name of 


Normal 


Symptoms of Defi- 


Innervated 


Represented 


which Muscle is 


Muscle. 


Function. 


cient Action. 


by 


in 


commonly In- 
volved. 


Triceps.... 


Exteuds fore- 


Arm cannot be ex- 


Musculo- 


Sixth, sev- 


1 Poliomyelitis 




arm; long 


tended except by 
its own weignt; if 


spiral. 


enth, eighth 
cervical seg- 


and other 




head of tri- 




affections of 




ceps, and cor- 


long head of tri- 




ments. 


cervical 




aco-brachialis 


ceps is affected 
subluxation f 






cord ; trau- 




help to keep 






matic inju- 




head f hu- 


head of humerus 






ries ; amyo- 




merus in posi- 


occurs easily. 






y t r op h i es 




tion. 








and dystro- 


Biceps 


Flexion and 


Flexion deficient, 


Musculo -cu- 


Fourth, fifth, 


phies (tri- 




supination of 


but can be carried 


taneous. 


sixth cervi- 


ceps es- 




forearm. 


out in part by 
other muscles. 




cal. 


c a p es in 
many pe 
r i phe r al 

. palsies.) 


Supin a 1 r 


Flexes fore- 


Flexion and prona- 


Muscu lo - 


Fourth, fifth 


As above ; in- 


longus. 


arm and aids 


tion deficient; 


spiral. 


cervical. 


volved in pe- 




in pronation. 


muscle does not 
stand out promi- 
nently if arm is 
flexed and a t- 






ripheral neu ■ 
ritis (traumat- 
ic), nob in 










lead palsy. 






tempt is made by 












another to extend 












it forcibly ; if mus- 












cle is atrophied 












arm i s spinule- 












shaped. 








Supinator 


Supinates 


Deficient supina- 


Muse ulo- 


Fifth cervi- 


Diseases as 


brevis. 


hand when 
forearm is ex- 
tended. 


tion of hand. 


spiral. 


cal. 


above ; also 
i n peripheral 
palsies. 


Extensor 


Extension 


Wrist cannot be 


Muse u 1 - 


Seventh cer- 


As before ; es- 


carpi ra- 


and abduc- 


flexed dorsally 


spiral. 


vical. 


peciall y in 


dialis 


tion of wrist; 


(extended) or ab- 






neuritis. 


longus et 


che shorter 


ducted ; flattening 








brevis. 


muscle has 
pure exten- 
s i n action 
only. 
Extension and 


of forearm. 








Extensor 


Wrist cannot be 


As above. 


Seventh cer- 


As above. 


carpi ul- 


abduction of 


flexed dorsally or 




vical. 




naris. 


wrist. 


adducted; "drop- 
wrist " is charac- 
teristic of paraly- 
sis of extensors. 








Extensor 


1 


First phalanges 


Musculo- 


Seventh cer- 


As above. 


d i g i t - 




cannot be ex- 


spiral. 


vical. 




rum com- 


Extension of 


tended nor fingers 








munis. 


| first pha- 


abducted ; grasp 








Extensor 


y langesofall 


is weak because 








indicis. 


fingers and 


flexor muscles are 








E x t e n sor 


abduction. 


shortened and 








minimi 




cannot contract 








digiti. 
Flexor 


1 

Flexion of 


forcibly. 
Deficient flexion. 


Median 


Eighth cer- 


As above. 


carpi 


wrist and pro- 






vical. 




radial is. 


nation. 










Flexor 


Flexion of 


Flexion and supi- 
nation impaired. 


Ulnar 


Eighth cer- 


As above. 


carpi 


wrist and 




vical. 




ulnaris. 
Palmaris 


supination. 
Flexion of 


Flexion impaired; 


Median 


Eighth cer- 


As above. 


longus. 


wrist only. 


no a n m a 1 ous 
position of hand 
from paralysis of 




vical. 


















wrist ashand falls 












by its own weight; 












the flexors f 












fingers may act as 












substitutes. 









THE NON-NEURONIC DISEASES 

Muscles of Arm, Forearm, and Hand. — Continued. 



641 













Diseases in 


Name of 


Normal 


Symptoms of De- 


Innervated 


Represented 


which Muscle is 


Muscle. 


Function. 


ficient Action. 


by 


in 


commonly In- 
vol /ed . 


Flexor 


Flexes second 


Second phalanx 
cannot be flexed. 


Median 


Eighth cer- 


As above. 


d i k i to- 


phalanx to- 




vical. 




rum sub- 


ward first. 










lines. 












Flexor 


Flexes last 


Last two phalanges 


Ulnar and 


Eighth cer- 


As above; 


d i g i to- 


two phalanges 


cannot be flexed. 


Median. 


vical. 


muscle should 


rum pro- 


toward first. 








be tested with 


fundus. 










special care 
i n cases f 
traumatic in- 
juries. 


Interos s e i 


Abduction and 


Fingers cannot be 


Ulnar, which 


Eighth cer- 


As above ; oft- 


and lum- 


adduction of 


abducted, or ad- 


also sup- 


vical, first 


en the first 


bricales. 


fingers if first 


ducted; inter- 


plies third 


dorsal. 


muscles to be 




phalanges are 


osseous spaces 


and fourth 




affected in 




extended; 


are very marked ; 


1 u m b r i- 




progressive 




flexion of first 


"Main en griffe " 


cales; medi- 




spinal atro- 




phalanges 


due to extension 


an supplies 




phies. 




and s i m u 1- 


of first phalanges 


first two and 








taneous e x - 


and flexion f 


so m e times 








tension of sec- 


Second and third 


third lum- 








ond and third 


phalanges. 


bricales. 








phalanges. 










Thenar 


Extends first 


Impairment of ex- 


Musculo- 


First dorsal. 


As before; 


muscles : 


phalanx and 


tension and ad- 


spiral. 




more espe- 


E x t e n sor 


abducts meta- 


duction ; flatten- 






cially in amyo- 
trophies and 


pol lici s 
brevis. 


carpal bone ; 


ing of ball of 






acts with ad- 


thumb. 






neuritis. 




ductor polli- 












cis longus. 










Extensor 


Extends both 


Deficient extension 


Musculo- 


First dorsal. 


As above. 


poll icis 
longus. 


phalanges of 


and adduction ; 


spiral. 






thumb ; also 


second phalanx is 










adduction of 


flexed toward 










metacarpal 


first. 










bone and 












backward 












movement of 












thumb. 










A b d uctor 


Abduction of 


Deficient abduc- 


M u scu lo- 


Fir6t dorsal. 


As above. 


poll icis 
longus. 


metacarpal 


tion of metacar- 


spiral. 






bone ; aids in 


pal bone ; if this 










flexion of 


muscle and ex- 










hand. 


tensor pollicis 
brevis are par- 
alyzed adduction 
results. 








Abductor 






Musculo- 






pollicis 
brevis. 






spiral. 
















Opponens 
pollicis 
and outer 


Opposition 
of thumb. 


No opposition 
movement. 


Median. 


First dorsal. 


As above. 


portion of 












the flexor 












brevis. 












Abductor 


Flex first pha- 


No flexion; if mus- 


Median and 




As above. 


pol 1 icis 
b r e vi 8 ; 


lanx and ex- 


cles are paralyzed 


ulnar. 






tend second 


and atrophied, 








flexor 


phalanx (like 


ape hand is 








brevisand 


i n terossei), 


formed. 








adductor. 


also have an 
abduction 
and adduc- 
tion action. 










Flexor 


Flexes end 


No flexion of end 


Median. 




As above. 


pollicis 


phalanx. 


phalanx. 








longus. 
















642 



THE NON-NEURONIC DISEASES 

Muscles of Back and Lower Extremities. 



Name of Muscle. 



Erector spinse; sa- 
cro-lumbalis; lon- 
gissimus dorsi. 

Abdominal muscles. 



Quadratus lumbo- 

rum. 
Adductor muscles. 

Sartorius. 

Quadriceps femoris. 



Ilio-psoas. 

Tensor fasciae lata?. 

External rotators: 
Pyriformis . 
Gemelli. 

Quadratus femoris. 
Internal obturator 
External obturator 



■Gluteal muscles. 

Biceps ; semitendi- 
nosus and semi- 
membranosus. 

Gastrocnemius (al- 
so plantarius and 
soleus). 

Anterior tibial mus- 
cles (tibialis anti- 
cus, extensor digi- 
torum, and exten- 
sor pollicis lon- 
gus). 

Peroneus longus. 



Posterior tibial mus- 
cle. 

Peroneus brevis. 

I n terossei pedis et 
lumbricales 

Adductor; flexor 
brevis and abduc- 
tor hallucis. 



Innervated by 



Dorsal nerves. Second to 
twelfth dorsal segments, 



Dorsal nerves. Second to 
twelfth dorsal. 



Lumbar nerves. 

Obturator nerve, great 
sciatic and crural. 

Crural. Third lumbar 
segment. 

Crural. Third lumbar. 



Crural (lumbar plexus). 

Fourth lumbar. 
Superior gluteal. Fourth 

lumbar. 

Sacral plexus (muscular 
branches). Fifth lum- 
bar. 

Obturator nerve (lum- 
bar plexus). 
Inferior gluteal (sacral 
plexus). First and sec- 
ond sacral. 
I Gluteal superior. First 
[ and second sacral. 
Sciatic. Fifth lumbar 
segment. 



Symptoms of Deficient Action. 



Internal popliteal, 
lumbar. 



Fifth 



Anterior tibial. Fifth 
lumbar and first sacral. 



Peroneal. First and sec- 
ond sacral segments. 

Posterior tibial nerve. 
First and second seg- 
ments. 

Peroneal. First and sec- 
ond segments. 

Posterior tibial. First 
and second segments. 

Posterior tibial. First 
and second segments. 



Lordosis of iower spine; perpendicular 
line from shoulder falls behind os sa- 
crum : unilateral palsy causes deflection 
of spine toward sound side. 

Lordosis with protrusion of nates and 
abdomen; other actions deficient; can- 
not straighten up from recumbent 
position without assistance of hands. 

Lateral movements of lower vertebra 
imperfect. 

No adduction; thigh rolls outward. 

Flexion impaired; acts imperfectly. 

Leg cannot be extended; to test it ask 
patient, who is lying down with hip 
bent, to stretch out the leg, when pa- 
tient is sitting down to extend leg. 

] Flexion difficult: in bed thigh cannot be 
J- flexed: difficulty rising from horizon- 
tal position. 



Deficient outward rotation 
inward. 



leg turned 



No extension of thigh: great difficulty in 
climbing; no abduction of thigh; wad- 
dling gait, exaggerated movement of 
pelvis. 

Deficient flexion; action of quadriceps 
may cause excessive extension ; in 
standing thigh is flexed to excess ; 
trunk moved backward. 

Deficient flexion of foot ; heel cannot be 
raised ; cannot stand on tiptoes. 

Deficient extension; " dropfoot," toes 
scrape floor ; to clear this, excessive 
flexion at knee and hip ; contracture of 
flexors and pes equinus or equinovarus. 



Deficient abduction ; plantar arch les- 
sened; increased by contracture. Flat- 
foot ; walking tiresome. 

I Deficient abduction or adduction , de- 
f fortuities result from deficiencies. 

Abduction and adduction of toes defi- 
cient ; paralysis of interossei ; hyp^rex- 
tension of first phalanges ; second and 
third flexed (clawed foot). 

Deficient flexion of toes ; foot cannot be 
pushed off ground easily. 



THE NON-NEURONIC DISEASES 643 



DISEASES OF THE CRANIAL NERVES. 

The olfactory and optic nerves, so-called, are parts of the brain 
and will be discussed in another part of the book. They are not 
nerves in the sense of being mere bundles of neuraxones remote from 
their ganglionic centers. They are part and parcel of the great intra- 
cranial ganglionic centers and tracts. The olfactory bulb is actually 
a cerebral lobe, and the optic nerves are pure cerebral tracts. 

The other cranial nerves are identical in structure with the spinal 
nerves. They spring from motor and sensory roots. The former have 
their cells bunched together in nuclei which are the mere forward ex- 
tension or homologous representation of the anterior horns of the 
cord. The latter have their cells collected in the ganglia (Gasserian, 
jugular, petrosal, geniculate, etc.) found on the roots of the sensory 
nerves. Like the spinal sensory nerves, the processes from these root- 
ganglion cells divide T-like, the peripheral end going out to the skin 
and special end-organs and the central end penetrating the medulla 
to terminate in arborizations in nuclei which are the homologues of 
the gelatinous substance of Rolando of the posterior horns of the cord. 

In one respect, however, the cranial nerves differ from the spinal 
nerves and thus obtain all their confusing arrangement. It is a mere 
non-essential anatomical difference, which is the result of the working 
of the great biological law of adaptation and in no way changes the 
physiology or physiological anatomy of the cranial nerves. 

The motor and cranial strands do not keep so rigidly apart and 
regularly arranged serially among the cranial nerves as they do among 
the spinal. 

The third, fourth, motor branch of the fifth, sixth, seventh, and 
twelfth are pure motor nerves. Their sensory correspondents are 
wrapped up together in the great trigeminal sensory nerve. This is 
shown by the study of the nuclei of origin of all these nerves. 

The ninth, tenth and accssory part of the eleventh belong to the 
visceral system and spring from nuclei on their roots while the motor 
parts originate in central gray matter that is homologous with the vesi- 
cular column of Clarke. The spinal part of the eleventh nerve is a 
pure spinal nerve. In some lower animals the twelfth, or hypoglossal 
nerve, is outside of the cranium entirely and in every respect simu- 
lates a spinal motor nerve. 

The important point in these biological observations to the prac- 
tical clinician is that diseases of these cranial nerves differ in no re- 
spect whatever from diseases of the spinal nerves. The essential 
differences in their semeiology depend entirely upon the organs and 
structures which they innervate. Disease of those thai go to the heart 
muscle will naturally awaken more significant manifestations than 
those that go to the face muscles. The symptoms that arise from dis- 
ease- of those that terminate in the ear will naturally be different from 
the symptoms of disease in those that end in the taste bulbs of the 
tongue. But the same holds true with the spinal nerves. From all 
points of view, therefore, the cranial nerves must be regarded in the 
same light as the spinal nerv 



644 



THE XOX-XEUROXIC DISEASES 



FIGURE 140. 
-A. Semibiagrammatic view of a deep dissection of the cranial nerves 
on the left side of the head (from various authors and from nature). B. Explan- 
atory outline of the same. (A.T.) \ 




The Roman numerals from I to XII indicate the roots of the several cranial nerves as 
they lie in or near their foramina of exit ; V, is upon the large root of the fifth with the 
Gasserian ganglion in front ; C I, the suboccipital or first cervical nerve ; C VIII, the 
eighth. The branches of the nerves are marked as follows, viz. : — 1, supraorbital branch 
of the fifth ; 2, lachrymal passing into the gland ; 3, nasal pausing towards the anterior 
internal orbital canal, and giving the long root to the ciliary ganglion, 4' ; 3', termination of 
the nasal nerve ; 4, lower branch of the third nerve ; 5, superior maxillary division of the 
fifth passing into the infraorbital canal ; 5', the same issuing at the infraorbital foramen 
and being distributed as inferior palpebral, lateral nasal, and superior labial nerves, 5" ; 
6, ganglion of Meckel and Vidian nerve passing back from it ; 6', palatine and other 
nerves descending from it ; 6", large superficial petrosal nerve ; 7, posterior dental nerves ; 
7', placed in the antrum, which has been opened, points to the anterior dental nerve ; 8, 
inferior maxillary division of the fifth immediately below the foramen ovale ; 8', some of 
the muscular branches coming from it ; 8-f , the auriculo-temporal branch cut short, and 
above it the small superficial petrosal nerve connected with the facial ; 9, buccal and ex- 
ternal pterygoid ; 10, lingual or gustatory nerve ; 10', its distribution to the side and 
front of the tongue and to the sublingual gland ; 10", submaxillary ganglion ; below 10, the 
chorda tympani passing forwards from the facial above 12, to join the lingual nerve ; 11, 



( From Quain. ) 



THE NON-NEURON1C DISEASES 



645 



FIGURE 140. 

inferior dental nerve ; 11', the same nerve and part of its dental distribution, exposed by - 
removal of the jaw ; 11", its termination as the mental nerve ; 11"', its raylo-hyoid branch ; 
12, twigs of the facial nerve immediately after its exit from the stylo-mastoid foramen. 



B. 




19" 



to the posterior belly of the digastric and to the stylo-hyoid muscle ; 1ST, temporo-facial 
division of the facial ; 12", c # ervico- facial division ; 13, trunk of the glosso-pharyngeal 
passing round the stylo-pharyngeus muscle after giving pharyngeal and muscular branches ; 
1H', its distribution on the side and back part of the tongue ; 14, spinal accessory nerve ; 
14', the same after having passed through the sterno-mastoid muscle uniting with branches 
from the cervical nerves ; 15, hypoglossal nerve ; 15', its twig 10 the tbyro-hyoid muscle ; 
1")", its distribution to the muscles of the tongue ; 16, its descending branch giving a 
direct offset to the anterior belly of the omo-hyoid muscle, and receiving the communi- 
cating branches 16 + , from the cervical nerves ; 1 7, pneumo-gastric nerve ; 17', its superior 
laryngeal branch ; 17", external laryngeal twig ; 18, superior cervical ganglion of the sym- 
pathetic nerve, uniting with the upper cervical nerves, and giving at 18' the superficial 
cardiac nerve ; 19, the trunk of the sympathetic ; 19', the middle cervical ganglion, 
uniting with some of the cervical nerves, and giving 19", the large or middle cardiac 
nerve ; 20, continuation of the sympathetic nerve down the neck ; 21, great occipital 
nerve ; 22, third occipital. 

(From Quain.) 



I 



646 



THE XOX-XEUROXIC DISEASES 



I will now discuss some of the more prominent diseases of them, 
thus continuing the discussion of the peripheral nerve diseases, part 
of which I have taken up in the previous section upon the spinal nerves. 

The diseases that involve the cranial nuclei and which produce 
ofttimes clinical pictures that cannot be sharply differentiated from the 
clinical pictures presented by disease in the respective nerve-trunks, 
will be considered among the affections of the medulla. In this I am 
following the same general plan as evidenced in the separation of the 
spinal nerve diseases from those of the gray matter of the cord. There 
is no logical congruity in separating, for instance, focal poliomyelitis 
from peripheral neuritis and throwing together ophthalmoplegia and 
peripheral ocular nerve palsies. 



OCULOMOTOR OR THIRD CRANIAL NERVE. 

This nerve, like the fourth and sixth nerves, arises from the 
nucleus in the floor of the aqueduct of Sylvius. It appears in the inter- 
peduncular space, passes forward to enter the orbit by the inner end of 
the sphenoidal fissure, and supplies all the muscles of the eyeball, ex- 
cept the superior oblique and the external rectus. Through the lenticu- 
lar ganglion it also supplies the sphincter muscle of the iris and the 
ciliary muscle. The elevator of the eyelid is also furnished with a 
branch. 

Etiology. — A general diathesis often underlies ocular palsy and 
the trouble is thus but a side manifestation of another, more extensive 
disease. With such an underlying diathesis, as, for instance, rheuma- 
tism, cold can play a very important part in initiating the local trouble. 
Sometimes the rheumatic, unilateral ophthalmoplegia has merely re- 
sulted from the extension of the disease from a focus somewhere in 
the neighborhood. 

Infection, especially diphtheritic infection, is responsible in some 
cases. The resulting neuritis may affect the whole or part of the nerve. 
The muscles of accommodation are particularly liable to be paralyzed. 
The sixth nerve often, the fourth rarely, is included in this form of 
palsy. It is not possible at times to distinguish this neuritis from nu- 
clear disease due to the same cause. Influenza, acute rheumatism, scar- 
latina, pneumonia, are some other forms of infection that have given 
rise to ophthalmoplegia. Tumors, thrombosis of the cavernous sinus 
and neighboring exostoses are in the etiology. Gummatous tumors 
and other syphilitic conditions at the base of the brain are all well 
known causes of ocular palsy. There is also a primary gummatous 
neuritis of the nerve itself. Toxccmia, such as occurs in alcoholism, 
lead-poisoning, and eating of tainted food (oysters, fish, meat, bologna) 
has been responsible in a few instances. In diabetes paralysis of the 
ciliary muscles and disturbances of accommodation are of common 
observation. The latter has been attributed to intestinal auto-intoxica- 
tion (Panas). Mydriasis was also present. Most of these cases, if 
not all of them, are better attributed to nuclear disease. 

Intracranial traumata need merely to be mentioned to be recog- 
nized as possible causes. Bone lesions in the orbit must not be over- 



THE XOX-XEUROXIC DISEASES 647 

looked. Fractures, aneurisms, tumors, exostoses, hemorrhages, ex- 
udates, are all liable to injure the nerve. 

Obstetrical (forceps) palsy, through pressure, has been seen in 
the oculomotor. Pressure of a damaging sort may be exercised other- 
wise also upon the nerve. 

In tabes, multiple sclerosis, and other general and intracranial 
diseases, oculomotor neuritis is uncommon. 

Symptoms. — Remembering the muscles supplied by the third 
cranial nerve, it is an easy matter to correlate the disease with the 
abnormal movements of the lid, eyeball and iris. 

Ptosis is a prominent symptom. The lid hangs down almost to 
the lower lid. The eye is not absolutely closed and the lid can be 
slightly raised because the fibres of the occipito-frontalis muscle ex- 
ercise some effect upon it. Place the hand upon the brow or get the 
patient to fix the occipito-frontalis and it will be very noticeable that 
he cannot move the lid a particle. 

As the internal rectus is innervated by the third nerve and the 
external by the sixth the ball of the eye cannot be rolled inward or 
made to follow the finger towards the nose. Only outward can the 
ball be moved. Contracture of the external rectus ultimately causes 
a downward, outward strabismus. Other movements of the ball are 
impossible. 

The iris remains a trifle larger than normal. It cannot contract. 
It dilates more rapidly than usual under atropine. Neither light nor 
convergence contracts it. 

Diplopia, slight exophthalmos and consequent disturbance of vis- 
ion result from the displacement of the line of fixation and relaxation 
of the affected muscles. 

Pains may accompany the rheumatic and compression form of 
the trouble. 

The above picture represents a total paralysis of the nerve. This 
usually is the case in peripheral disease, though not always so. In 
nuclear disease there is more frequently a separation of the internal 
from the external ophthalmoplegia. A bilateral palsy of the sphincter 
iridis and ciliary muscle, or a bilateral external palsy with retention 
of accommodation is almost pathognomonic of central disease. Per- 
ipheral disease may be inferred when neighboring cranial nerves are 
affected. 

Though it is impossible of actual demonstration we assume that 
the paralysis is atrophic and flaccid, as in all peripheral palsies. 

There is a recurrent or periodical ocular palsy that should re- 
ceive some mention here. Cases have been seen by Saundby, Snell, 
Gubler, Mobius, Senator, Buzzard, Pfliiger, Charcot, Manz, ( )ppen- 
heim and others. 

Every few days, weeks or months the eyelid falls and remains 
down for a variable time. The trouble is mostly unilateral. With the 
paralysis there has been headache, pain in the eyeballs, nausea and 
vomiting. The disease is supposed to be related to migraine, though 
it is not strictly identical with it. It may last a week. The whole 
nerve is usually involved. Albuminuria has accompanied it. Both 






648 



THE NON-NEURONIC DISEASES 



sexes are subject to it and it has been seen in children. Female adults 
are more frequently its victims. It is a mysterious trouble and noth- 
ing is known of its cause. The most plausible hypothesis is that of 
Charcot who likens the disease to hemicrania. 

Prognosis. — This is entirely dependent upon the cause. Infec- 
tious cases as a rule recover. Properly treated syphilitic cases offer 
most favorable prognoses. Less favorable, but still not absolutely bad, 
are the traumatic cases. If the nerve is not too severely damaged and 
the cause can be removed the outlook is good. Inoperable brain tumors 
of course render the accompanying ocular palsy hopeless. Tabetic 
ocular palsies usually recede, though not always. The prognosis of 
an isolated iridoplegia is grave because it may be the advance sign of 
tabes or general paresis. It occurs, however, in alcoholism and syph- 
ilitic cerebral disease and under treatment may recover. 

Treatment. — First, remove the cause as promptly and completely 
as possible. If rheumatism, syphilis, influenza, diphtheria or other 
infection is present it must be attacked with the usual medicines. 
Sweating must be encouraged. General antiphlogistic treatment, with 
local vesication and bloodletting, must be instituted. Later on electrical 
treatment may be tried, though it is not very effective. Galvanism is 
the best current to use, with the cathode on the back of the neck and 
the anode directly over the eye. The electrodes may be placed up on 
the opposite temples. The seance should be only three or four minutes 
and the current just strong enough to contract the facial muscles. 
Faradism should never be used. 

Hypodermics of strychnine are often of much benefit. Prisms 
and protectors over the affected eye may give relief from the double 
vision. Ophthalmic surgery has been resorted to for overcoming the 
ptosis. 

TROCHLEAR, PATHETICUS, OR FOURTH CRANIAL 

NERVE. 

This is the smallest of the cranial nerves and yet has a long course. 
It springs from the nucleus in the floor of the aqueduct of Sylvius. It 
emerges from just beneath the corpora quadrigemina, curves outward 
around the superior peduncle of the cerebellum and the outer side of 
the crus cerebri, passes forward in the outer wall of the cavernous sinus 
and into the orbit by way of the sphenoidal fissure, and ultimately termi- 
nates in the end-plates of the superior oblique muscle. 

Paralysis of this muscle causes the eye to turn slightly inward 
when looking down. There may be diplopia in the lower half of the 
visual field. It is noticeable when the patient descends a flight of steps, 
all of which seem to be double. 



THE ABDUCENS, OR SIXTH CRANIAL NERVE. 

This nerve also originates in the nucleus in the floor of the aque- 
duct of Sylvius. It supplies the external rectus of the eyeball and thus 
is appropriately considered in connection with the previous two nerves. 



THE NON-NEURONIC DISEASES 649 

It is, of all the cranial nerves, the one most frequently diseased. This 
is largely on account of its long, exposed course at the base of the 
brain. Emerging just behind the pons Varolii above the pyramids, it 
passes forward close to the floor of the cavernous sinus, enters the orbit 
through the sphenoidal fissure and terminates in the external rectus.. 
Its paralysis results in internal strabismus and limitation of ex- 
ternal movements of the eyeball. Diplopia is present and may be 
homogeneous. The head is usually turned towards the side of the 
paralyzed muscle. Gummatous disease particularly attacks the abdu- 
cens nerve. 

TRIFACIAL, TRIGEMINAL, OR FIFTH CRANIAL NERVE. 

This is a combined motor and sensory nerve. The motor root 
springs from a nucleus in the floor of the fourth ventricle and the 
Sylvan aqueduct. The sensory root, which represents the central 
processes of the neurones whose cell-bodies are in the Gasserian 
ganglion lying on the petrous part of the temporal bone, is traceable 
under the superior cerebellar peduncle in the pons to the nucleus of 
Rolando in the medulla. 

Starting from the sides of the pons Varolii, nearer its upper than 
its lower border, the small or motor root lies at first above the large 
or sensory one. Both branches then pass forward to the middle fossa 
of the skull, enter a recess of the dura over the summit of the petrous 
bone, where the ganglion in the sensory portion of the nerve is found. 
The motor trunk passes beneath the ganglion to join the lowest of the 
three branches of the ganglion just below the foramen ovale. The three 
branches that project from the Gasserian ganglion are the ophthalmic, 
which enters the orbit and emerges in the terminal supra-orbital nerve 
that runs up on the forehead ; the superior maxillary, which is continued 
foiward to emerge from the supra-maxillary foramen between the 
orbit and the mouth ; and the inferior maxillary which is distributed to 
the external ear, the tongue, the lower teeth and by the branch that 
emerges from the infra-maxillary foramen in the lower jaw\ The 
motor branch terminates in the muscles of mastication, namely, the 
temporal, the massetcr and the two pteragoids. 

This is the great sensory nerve of the face, probably the most 
important sensory nerve in the body. It imparts common sensibility 
to the face, the fore part of the head, the eye, the nose, the ear and 
the mouth, including the greater portion of the tongue. To the ante- 
rior two-thirds of the latter it is believed to confer the power of 
taste, the taste fibres coming really from the glossopharyngeal by way 
of the facial and the chorda tympani. 

In the orbital cavity, fibres from the sympathetic nerve run along 
beside the ramus ophthalmicus of the fifth nerve and innervate the 
dilator muscle of the pupil, after emerging from the ciliary ganglion. 
To the second branch of the fifth is attached the spheno-palatine gan- 
glion which is connected with the geniculate ganglion of the facial 
nerve by the Vidian, or large superficial petrosal nerve. 

To the third branch is attached the otic ganglion, which also is 



650 



THE N0N-NEUR0NIC DISEASES 



connected with the geniculate ganglion of the facial by the small super- 
ficial petrosal nerve. This last nerve sends a branch, Jacobson's tym- 
panic nerve, to the glosso-pharyngeal. 

The innervations of the trigeminal nerve have lately been seen 
to be very variable. 

Not often does isolated disease of this nerve occur. The nature 
of its neuralgic manifestations have been described under the head of 
neuralgia elsewhere. 

Etiology. — Neighboring bone disease, caries, exostoses, tumors, 
chronic meningitis and syphilitic disease have damaged the nerve. I 
have lately seen a case of gummatous neuritis in it. Traumata and 
infection, especially rheumatism, have been responsible for its disease in 

FIGURE 141. 




Course of the facial nerve and its anastojnoses with the trigeminal and glossopharyngeal nerve* 

(After Leube.) 

some cases. Surgical operatiojis in and about the orbit and maxillary 
bones are to be included sometimes in the etiology. I have seen the 
nerve manifest paralytic s) mptoms in cases of ear disease. As a col- 
lateral trouble in brain tumor, hemorrhage, pontile encephalomalacia, 
tabes and syringomyelia, disease of the trifacial is not an uncommon 
event. 

Symptoms. — The symptoms depend upon the character and loca- 
tion of the lesion. If one remembers the physiological anatomy of the 
nerve, the symptoms may easily be inferred. Motor, sensory and 
trophic manifestations occur in total paralysis of the nerve. 

The jaw cannot be closed, nor moved laterally as it is slightly, in 
chewing food. The anaesthesia involves the face in front of a line 
passing transversely across the top of the head, down through the 
external auditory meatuses and along the lower edge of the lower 
jaw. The accompanying diagram, with figures corresponding with 
the branches of the nerve, will show its cutaneous distribution better 



THE XOX-XEUROXIC DISEASES 



6;i 



than a long description. In this area should be included the mucous 
membrane of the nose, mouth, tongue, gums and inside of the cheek ; 
also the conjunctiva and the cornea. On account of the insensitive- 
ness of the cornea, winking is not performed as systematically as it 
should be and it becomes irritated from minute particles of matter. 
The secretion of tears being impaired adds to this misfortune. Vision 
is blurred slightly. Smell and taste are blunted on account of the dry 
■condition of the mucous membrane of the nose and mouth. Often the 
cheek is bitten and lacerated internally in the process of chewing. 

We do not know yet just exactly the nature of the role played 
by the trigeminal nerve in the matter of taste. Many believe that the 
fibres of the third branch which subserve the function of taste in the 
anterior two-thirds of the tongue are wholly from the glosso-pharyn- 

FIGURE 142. 




Cutaneous area of the head supplied by the trigeminal nerve. 

geal. albeit they have come by way of the facial and chorda tympani 
nerves. This being so, the glosso-pharyngeal nerve is the nerve of 
taste for the whole tongue. However, it is true that taste depends 
largely upon the ordinary sensory and trophic condition of the mu- 
cous membrane, and in maintaining this in a normal state, the essential 
fibre> of the trifacial nerve, those that come from the Gasserian gan- 
glion, subserve in part the function of taste. At all events gustatory 
disturbances occur in the anterior two-thirds of the tongue when the 
fifth nerve or its inferior maxillary or lingual branches are injured. 

Herpes is a common trigeminal symptom. Indeed the trophic 
symptoms of disease of this nerve or its branches are among the most 
important. In neuroparalytic keratitis, the vision is badly blurred: the 
cornea ulcerates; perforation takes place; the whole eye inflames 
(panophthalmitis). This is a pure trophic trouble and not due solely 
to anaesthesia as was formerly thought, ft is not neuroparalytic lint 



652 



THE NON-NEURONIC DISEASES 



neuritic in origin. Ulceration also occurs, as a trophic symptom, in 
the cheek and nose. The teeth loosen and fall out, though this is 
due more to central disease. Some authorities believe that progressive 
facial hemiatrophy is a trophic disease of the trigeminal nucleus. 

As in all neuritic palsies these are flaccid in type, the temporal, 
masseter and pteragoid muscles atrophy and when they can be exam- 
ined the electrical reaction of degeneration is found. The jaw re- 
flex, of course, is absent. In unilateral palsy the immobility of the 
jaw is not so noticeable. If the patient is asked to press the teeth- to- 
gether and then still more compress the jaws, it will be noticed that 
the muscles do not contract on the paralyzed side. 

Instead of signs of paralysis there may be signs of irritation. 
Parcesthesice then are in the lead and pains and excessive secretion. 
There may be a facial spasm and, through reflex irritation, coughing, 
sneezing, vertigo, etc. 

The prognosis of course depends upon the nature and location of 
the lesion. If the cause of the inflammation or irritation can be re- 
moved, recovery may be expected. 

Treatment. — The cause must be removed and to a large extent 
this exhausts the treatment. Syphilis is so prolific a cause that antispe- 
cific treatment should be persevered in, even if immediate results are 
not forthcoming. I have had good results from such a mode of pro- 
cedure. The eyes should always be protected. For pains, analgesics 
and electrotherapy are our only resources. Surgery may accomplish 
much if the indications are clear enough. It is questionable whether 
the risk of producing trifacial neuritis, as is possible in the injection 
of perosmic acid, will be warranted by the suffering sometimes caused 
in pure trifacial neuralgia. The latter is fearful at times, but the 
former has destroyed vision and caused facial atrophy, paralysis and 
other severe manifestations. 



THE FACIAL, OR SEVENTH CRANIAL NERVE. 

This is a pure motor nerve, whose nucleus is in the floor of the 
fourth ventricle beneath the superior fovea. It appears at the upper 
part of the medulla in the groove between the olivary and restiform 
bodies, close to the lower edge of the pons. Outside of it is the audi- 
tory nerve with a strand, the pars intermedia of Wrisberg, arising in a 
nucleus beneath the inferior fovea and connecting with the auditory. 
The facial, auditory, and pars intermedia all enter the internal auditory 
meatus together. At the bottom of the meatus, however, the facial 
parts company from the others and enters the aqueduct of Fallopius, 
following the windings of the canal through the temporal bone to the 
stylo-mastoid foramen. In the canal it gives off two important branch- 
es, the chorda tympani, which seems to be a taste nerve, and unites 
with the lingual branch of the fifth to innervate the anterior two-thirds 
of the tongue, and the branch to the stapedius muscle. After its 
emergence from the skull, the main trunk of the nerve passes down- 
wards and forwards through the parotid gland and terminates by 
dividing just behind the ramus of the jaw into the temporo-faciat 



THE NON-NEURONIC DISEASES 653 

above and the temporo-ccrvical below, each of which sends numerous 
branches to the side of the head, the face and the upper part of the 
neck. As these branches inter-communicate freely, they form a sort 
of a plexus which is often called the pes anserinus. As the muscles 
to which these filaments go, namely, the buccinator and all those of 
the face except the muscles of mastication, play so prominent a role in 
•expression, the facial is sometimes called the "artist's nerve." 

To briefly recapitulate, the facial nerve is distributed to the mus- 
cles of the seal p. of the external ear, nose, mouth, eyelids (excepting 
the levator palpebral superioris) and to the platysma. It also supplies 
the muscles of the tympanum, the levator palati and azygos uvulae 

FIGURE 143. 

— The facial nerve 
ii its canal, with its con- 
NECTING branches, &c (from 
Sappey, after Hirschfeld and 
Leveille). 3 

The mastoid and a part of the 
petrous bone have been divided 
nearly vertically, and the canal of 
the facial nerve opened in its 
whole extent from the internal 
meatus to the stylo-mastoid fora- 
men ; the Vidian canal has also 
been opened from the outside : 1, 
facial nerve in the first horizontal 
part of its course ; 2, its second 
part turning backwards ; 3, its 
vertical portion ; 4, the nerve at 
its exit from the stylo-mastoid 
foramen ; 5, geniculate ganglion ; 

6, large superficial petrosal nerve ; 

7, sphenopalatine ganglion ; 8, small superficial petrosal nerve ; 9, chorda tympani ; 
10, posterior auricular branch cut short ; 11, branch to the digastric muscle ; 12, branch 
to the stylo-hyoid muscle ; 13, twig uniting with the glosso-pharyngeal nerve (Hand 15). 

< through the large superficial petrosal) and the stylo-hyoid and the 
posterior belly of the digastric. 

It is well to remember its wide inter-connection with other nerves. 
It is thus associated with the fifth nerve, with the spheno-maxillan , 
submaxillary and otic ganglia, with the auditory, the glosso-pharvn- 
geal and pneumogastric nerves (through the auricular branch of the 
latter ) and with parts of the sympathetic and spinal nerve-. 

Prosopoplegia. or facial palsy, is the most common of the nerve 
paralyses. We are here only concerned with the peripheral type. 
though the disease may be of central and cortical origin. 

ETIOLOGY. — Exposure to cold is the time-honored cause of Bell's 
palsy. It is thus sometimes spoken of as rheumatic or refrigeratory 
palsy. It often follows sleeping beside- an open window, working in 
winter on a derrick with the head, all but the face, completely covered. 
Car-drivers, expressmen, and persons so exposed are liable. It is ac- 
knowledged that cold alone can produce the disease in healthy individ- 
uals. However, it must not be forgotten that in a very large number 
of the cases, cold only acts conjointly with some underlying infection. 







654 



THE NO N- NEURONIC DISEASES 



Lately I have treated a syphilitic sewing-girl whose face became par- 
alyzed on one side after sitting in a cold draught of air blowing in 
through an open door. It follows local infectious processes in and 
about the temporal bone. Caries and otitis media and tonsillar angina 
have started it. It is not improbable that both diseases may be simul- 
taneous products of the same general infection. It has followed thus, 
typhoid, mumps, and influenza. Syphilis has been a prolific source of 
the trouble in my observation, notwithstanding the fact that some au- 
thors say that of all the nerves of the body, syphilis respects most the 
facial. It occurs in diphtheria and the puerperium. 

Diabetic conditions are often responsible for it ; such as diabetes, 
gout, leukemia. 

Compression paralysis often attacks the nerve in basal gumma- 
tous meningitis. This is a common cause and must be distinguished,, 
by other signs of the basal disease, from the syphilitic neuritis re- 
ferred to above. Other forms of meningitis, as well as intracranial 
tumors, aneurisms, etc., may compress the nerve deleteriously. Trau- 
mata must not be omitted from its etiology. Not infrequently oper- 
ations about the ear are responsible for the paralysis. Bilateral dis- 
ease may occur in the polyneuritides and a diplegic facial paralysis 
may be the symptom of pontile and medullar disease, such as tumor,, 
hemorrhage, embolism, aneurism. It has occurred in tetanus. Pre- 
natal or natal damage may result from the use of the forceps. I once 
saw a severe facial palsy of this sort. This is called congenital facial 
paralysis and is usually bilateral. Some of these congenital palsies 
are undoubtedly nuclear in origin, as also are some of the diphtheritic 
cases. In many instances a pronounced neuropathic state of the con- 
stitution lurks behind it. 

Symptoms. — The cardinal symptom, paralysis of the face, is ob- 
vious enough. In fact, it is so obvious that the diagnosis of facial 
palsy does not confer a spark of credit upon the practitioner. Every 
newsboy can diagnose facial palsy when he sees it. To the physi- 
cian falls the duty of localizing the lesion, and therein lies the cred- 
itable diagnosis. 

The appearance of the face is typical and striking. On the 
paralyzed side it is smooth, dead and mask-like. The creases of the 
forehead on that side are gone ; so also are the naso-labial fold and 
the wrinkles of the cheek and chin. The corner of the mouth droops, 
the eye is almost completely open. If the patient attempts to whistle 
or laugh or show his teeth, or draw the mouth over toward the 
paralyzed side, the paralysis of the orbicularis oris is especially notice- 
able. 

If he is asked to close his eyes, the well side closes promptly but 
the affected side remains open or the upper lid moves slowly and only 
slightly towards the lower lid. 

On account of the failure of the buccinator to hold the bolus or 
food between the teeth, chewing is difficult and in bilateral paralysis 
all but impossible. Sometimes a slight swelling o\ the face accom- 
panies these motor manifestations. Occasionally for several days be- 
fore their onset there will be fugitive pains in the car, face or neck. 



THE NON-NEUBON1C DISEASES 655 

The asymmetry of the face in this disease is the pathognomonic 
feature. The eyes water, the conjunctiva bulges, the nose inclines 
toward the well side and saliva tends to drool from the mouth. Upon 
attempted movement this is rendered more marked. The muscles of 
the ear are implicated, also the platysma. There is some doubt as to 
the implication of the uvula in pure peripheral palsy. Occasionally the 
arch of the palate is lower on one side. As the disease involves usu- 
ally that part of the nerve in the aqueduct of Fallopius, the paralysis 
of the stapedius causes hyperacuity of the hearing; and of the chorda 
tympani, disturbance of the taste in the anterior two-thirds of the 
tongue. The latter is a form of hemiageusia. Rarely it may be total. 
Anosmia may occur from lessened dilatation of the nostril. 

Salivary secretion is diminished on the diseased side. This is 
one of the vasomotor or secretory effects of the nerve. 

The tongue is not implicated as that is under the control of the 
twelfth nerve. 

Among the trophic manifestations of facial disease are cedema- 
tous swelling previously mentioned, the herpetiform eruptions and the 
degenerative muscular changes. The former are rare ; the latter com- 
mon. The reaction of degeneration is an important symptom as it 
helps to determine the prognosis. The lid reflexes and skin reflexes 
are lost, of course, where the arc involves, on the motor side, the 
paralyzed muscles. 

Diagnosis. — The most important point of the diagnosis is the 
location of the lesion. The disease may be central or peripheral. If 
it is peripheral the flaccidity of the palsy, the muscular atrophy, the 
reaction of degeneration and the loss of the reflexes will go far to de- 
termine it. In many cases, however, the paralysis is only partial and 
these signs are not pronounced enough to form a positive opinion upon. 

The distribution of the paralysis is an important and valuable 
means in differentiating central from peripheral facial disease. In 
peripheral disease the whole nerve is implicated and hence the upper 
and lower part of the face are equally affected. In central disease the 
upper part of the face is very much less affected than the lower. This 
is very noticeable in hemorrhagic apoplexy. 

The path from the facial center in the cerebral cortex to the facial 
nuclei in the medulla is not very well known, though we believe it 
joins that of the arm and leg and passes down through the internal 
capsule of the pyramidal tracts in the crura cerebri. It decussates. 
This is the volitional facial tract. When the lesion is anywhere in 
this part of the tract, the upper facial is intact (probably because oi 
the bilateral cerebral representation) ; the reflexes and electrical ex- 
citability are normal. The muscles tend to spasticity and there is 
no atrophy. Usually the extremities are paralyzed at the same time. 
If the lesion should be a small one and attack this upper facial path- 
way between its point of decussation in tin- pons and its termination 
in the nucleus, the paralysis in relation to the face and limbs will 
obviously be a crossed paralysis. 

The localization of the lesion in peripheral disease of the nerve is 
often important and usually not difficult. Traumatic causes often g 







656 



THE NON-NEURONIC DISEASES 



rise to disease of particular branches. A knowledge of the anatomy of 
the nerve is all that is necessary tinder such circumstances to settle 
which branch is affected. 

It is difficult at times to differentiate between pontile facial palsy 
and palsy due to the peripheral trunk. A close examination will usu- 
ally elicit other manifestations of the disease of the pons under such 
circumstances. Other nerves may be involved, especially the sixth 
and sometimes the seventh. 

In meningitis and other basal disease implicating the facial nerve, 
other nerves will also very likely be included, especially the auditor}-. 

FIGURE 144. 




Showing the facial trunk from the base Of the 
skull to the pes ansennus. N.f., facial nerve , F.st., 
stylomastoid foramen N.a.p., posterior auricular 
nerve N.p.s., greater sup. petrosal nerve , N.e.c.p.t., 
communicating nerve, with plex tymp. , N.sl , sta- 
pedius nerve, Ch.t., chorda tympani , N.n., acoustic 
nerve. G.g., gangl. geniculi. (After Erb.) 

Of course, general cerebral symptoms would be expected also, such as 
pressure headache, vertigo, vomiting, possibly papillitis. 

If the lesion is peripheral to the point where the chorda tympani is 
given off, and central to that where the temporo-facial and temporo- 
cervical separate, only the facial muscles will be paralyzed. 

If the lesion is in the aqueduct of Fallopius the chorda tympani and 
stapedius branches will be implicated and there will be loss of the 
sense of taste in the anterior two-thirds of the tongue and a hypersensi- 
tiveness of the hearing. Erb's diagram helps to make this clear. Vari- 
ations are possible, however. 

Prognosis. — Mild cases usually get well in three or four weeks. 
Three to six months are required for the average case. Severe cases 
do not get well uncbr a year and sometimes they remain stationary. 



THE XOX-XEURONIC DISEASES 657 

Of course, the cause and nature of the lesion regulate the prog- 
nosis. If the cause is removable early, the disease will disappear. 
Syphilitic cases are very hopeful. Simple refrigerator)- cases are favor- 
able. Severe infectious cases, and those due to intracranial neoplasms, 
are often hopeless. 

The degree of reaction of degeneration is a most valuable indi- 
cator of the prognosis and probable duration of the disease. If this is 
partial, the trouble may disappear in a few weeks. If this is complete, 
the end may not come for many months or years even. Acute cases are 
better than the slow, chronic and progressive cases. 

A secondary trouble of much moment are the contractures that oc- 
cur late in the previously paralyzed muscles. These are not due to 
electrical treatment, as was once imagined. They are due to the irrita- 
tion of the nucleus in the forcible attempts at the use of the nerve, or 
to slight secondary nuclear alterations. 

Sometimes recovery is incomplete, some muscles regaining their 
power and others remaining palsied. 

Treatment. — The first indication of course is to remove the 
noxious agent. Infections, like rheumatism, syphilis, influenza, must 
be combated along known lines. Abscesses must be drained. Ear 
disease should be treated. A general and local antiphlogistic treatment 
is usually in order. This includes purgation, blood-letting, warm ap- 
plications beneath the ear, vesication, diaphoresis. 

When active inflammation has subsided, electrical treatment is 
called for and gives most happy results. The galvanic current usually 
has to be employed first. The anode is placed on the sternum or other 
indifferent spot, while the cathode is placed on the nerve trunk where 
it emerges from the stylo-mastoid foramen. For two or three minutes 
daily, three or four milliamperes may be employed in a slow, alternating 
current. Never use strong currents, also be careful about usin'g the 
faradic current in severe cases. 

Secondary contractures cannot be combated by any known means. 
Massage may help some. 

THE AUDITORY, OR EIGHTH CRANIAL NERVE. 

This is a nerve with a double function, both sensory. It subserves 
hearing and the space-sense. It arises from three nuclei in the floor of 
the fourth ventricle and emerges from the groove between the pons 
and the medulla. The nerve passes with the facial to the internal audi- 
tory meatus. In the meatus it separates into an upper, or small, and a 
lower, or larger, part. The upper goes to the utricle and the ampullae 
of the superior and external semicircular canals. The lower innervates 
the organ of corti in the cochlea, sending off small twigs to the saccule 
and the posterior semicircular canal. It is in connection with the pars 
intermedia and the geniculate ganglion of the facial. 

Disease of this nerve does not occur often in the isolated form. 
Middle ear disease often extends to the terminal branches of the nerve 
in the labyrinth. Meniere's symptoms are thus explained. In my own 
opinion, some of the so-called cases of Meniere's disease are central 



658 THE NON-NEURONIC DISEASES 

troubles, as I have shown elsewhere. Caries, periostitis, tumors, menin- 
gitis, infections, cachexia? and all the usual causes cited in connection 
with facial nerve palsy may be operative here. General degenerative 
troubles, like tabes, multiple sclerosis, alcoholic neuritis, may include 
the auditory nerve. Syphilis I have seen cause trouble in it many 
times. This was probably due to gummatous meningitis. Labyrinthine 
and auditory disease cannot always be differentiated, which is one of 
the grounds of my contention that Meniere's syndrome is far from be- 
ing a definite disease, hemorrhagic or otherwise. Basal disease usually 
involves the facial along with, or more often apart from, the auditory 
nerve. 

In every case of aural vertigo, of tinnitus and of disturbance of 
hearing, the ear should be thoroughly examined. Subjective tinnitus 
and subjective deafness may occur in so many other functional and 
organic diseases that the implication of the auditory nerve had better 
be made by exclusion. 

The prognosis and treatment of auditory paralysis follow the usual 
principles. 

THE GLOSSOPHARYNGEAL, OR NINTH CRANIAL NERVE. 

The roots of this nerve are traceable back to a nucleus which is 
closely associated with that of the vagus nerve, and which lies in the 
floor of the fourth ventricle in the posterior triangle beneath the in- 
ferior fovea. It appears at the upper part of the medulla, in the groove 
between the olivary and restiform bodies. It is directed outwards to the 
jugular foramen. Passing through this in company with the pneu- 
mogastric and spinal accessory, it presents two ganglia, the jugular and 
the petrous. The nerve lies between the internal carotid artery and the 
jugular vein. It courses down over the artery and beneath the styloid 
process and the muscles connected with it, to the hinder border of the 
stylo-pharyngeus. Crossing the outer surface of this muscle and pass- 
ing beneath the hypoglossus, it ends in a number of branches to the 
posterior part of the tongue. It supplies the mucous membranes of the 
tongue, pharynx and middle ear, as well as one muscle, the stylo- 
pharyngeus. It is connected with the inferior maxillary division of the 
fifth nerve (through the otic ganglion), the facial, the pneumogastric 
(its trunk and branches) and the sympathetic. 

This is regarded as preeminently a nerve of taste. We know so 
little about it, however, that nothing can be said positively in regard to 
its physiology or pathology. It has motor fibres, as we have seen, and 
it certainly conducts sensations of simple touch. The nerve may be 
implicated, like any other cranial nerve, with tumors, traumata, aneu- 
rism, neighboring inflammation. Thrombosis of the jugular vein ami 
periphlebitis may affect it. It is subject to degeneration as a part of 
a most extensive process. 

Its paralysis causes ancesthesia, ageusia in the posterior third of the 
tongue and palate and dysphagia. Diphtheria causes some of these 
symptoms. 



THE NON-NEURONIC DISEASES 659 

THE PNEUMOGASTRIC, OR TENTH CRANIAL NERVE. 

The roots of this nerve can be followed back to the trigonum vagi 
in the floor of the fourth ventricle. The nucleus ambiguus is believed to 
be the origin of the motor strands. The sensory roots represent the cen- 
tral processes of the neurones whose cell-bodies lie in the ganglion of 
the root and of the trunk. These processes enter the medulla and de- 
scend with those of the glosso-pharyngeal root, arborizing around cells 
which make up the so-called vagus, sensory nucleus. It is very probable 
that these cells of the terminal nuclei of this and the ninth nerve are but 
homologues of those making up the vesicular column of Clarke. Both 
the motor and sensory fibres of this nerve are distributed to viscera 
chiefly. 

The roots appear in the groove between the olivary and restiform 
bodies. This nerve has the largest course of any of the cranial nerves, 
reaching from the neck to the upper part of the abdomen. It passes 
outward from the medulla, attains the jugular foramen,, presents two 
ganglia, is joined by the accessory part of the spinal accessory nerve 
and finally passes on down the neck and thorax and abdomen dis- 
tributing branches to the lungs, the heart and the other viscera. 

In the jugular foramen, a branch is given to the dura mater and 
one to the ear. In the neck the pharnyx, larynx and the heart are sup- 
plied. In the thorax, branches are furnished to the heart, the lungs 
and the oesophagus. In the abdomen the terminal branches are given 
to the stomach, the liver and other organs. Motion, sensation, secretion 
and vasomotor action are all under the influence of the vagus. 

A primary neuritis of this nerve is very rare, if it occurs at all. 
Disease of any other structure along its course may damage it 
in that neighborhood, however, and in this way the nerve is not in- 
frequently affected. Primary inflammation of the nerve has been ob- 
served in rheumatism, alcoholism, diphtheria, typhoid, pneumonia, 
scarlatina, malaria, cholera, influenza. Under these circumstances it 
has usually constituted a part of a polyneuritis. I recently saw it 
affected in chronic lead-poisoning to a dangerous degree. Arsenic 
will injure it. Morphine and atropine may intoxicate it. 

It is usually implicated in bulbar disease. Disease at the base of 
the skull constitutes an important factor in etiology. This includes 
caries, exostoses, tumors, aneurisms, hemorrhages, meningitis with 
exudates. 

Numerous are the vascular troubles that disturb it, such as arterio- 
sclerosis, thrombosis of the transverse sinus, jugular thrombosis and 
phlebitis. Mediastinal tumors, suppuration, tuberculous glands, peri- 
carditis, and wounds and operations in the neck and thorax must all 
be sometimes reckoned with. 

Not only are vagus symptoms associated with tabes and multiple 
sclerosis but they also appear in hysteria and other neuroses. 

Symptoms. — A total vagus paralysis may occur from basal dis- 
ease, but it is not common. ( Hlier cranial nerves are usually implicated 
at the same time. The eleventh, ninth and twelfth are thus usually 
included. 






660 THE NON-NEURONIC DISEASES 

The symptoms of vagus palsy usually assume characteristics in 
accordance with the particular location of the lesion. Phonation is 
affected and the palate, larynx and fauces are seen to be paralyzed. 
On account of the condition of the palate the speech, of course, is nasal. 
Dysphagia is present. The respiration is disturbed. Rarely there 
has been anaesthesia of the pharynx and larynx. 

Acceleration of the heart action is an old and well-known symp- 
tom. The inhibitory control of the nerve over the heart is one of the 
ancient teachings of physiology. In unilateral lesions the heart has 
been seen to be retarded. Irritative lesions may exaggerate the in- 
hibition and so retard the cardiac phenomena. 

Respiratory disturbance, bulimia, vomiting, absence of hunger 
and thirst, pain in the stomach and diabetic manifestations are all to 
be attributed to vagus trouble sometimes. The respiratory implication 
results usually in what is called aspiration pneumonia, or hypostatic 
congestion of the lungs. 

Laryngeal paralysis is especially significant. It may occur alone 
or as a part of a general vagus palsy. These cases belong to laryngol- 
ogy. I have under my care a syphilitic with complete paralysis of the 
right vocal cord. Spasmodic coughing, embarrassed breathing and 
alteration of the voice are all among the symptoms. In bilateral palsy, 
there is complete aphonia, inspiratory stridor and dyspnoea. This oc- 
cus in diseases of the medulla usually and not infrequently in hysteria. 
I saw it lately as a neurosis following a lightning stroke. As a neurosis 
phonation is much more affected than respiration, whereas in organic 
disease respiration is dangerously involved along with the loss of 
voice. The reason is obvious for respiration is a function much farther 
removed from the volitional cerebral functions than is phonation. 

Paroxysmal tachycardia, asthma nervosum and partial paralysis 
of phonation may all be observed. 

Treatment. — Seach for and remove the cause. Syphilis especially 
must be attended to. Alcohol, tobacco and other toxins must be re- 
moved. Lead should be eliminated in the usual way with baths, purga- 
tives and the iodides. Supporting diet must be urged. 

Electrical treatment has not proved of much benefit in my hands, 
though it is well always to try it. External applications are better than 
direct applications in the larynx. 

There is a massage of the larynx. 

Tracheotomy may have to be resorted to in some dangerous cir- 
cumstances. 

THE ACCESSORIUS, OF ELEVENTH CRANIAL NERVE. 

A part of this nerve, the accessory, belongs practically to the vagus 
system and physiologically cannot be separated from it. The spinal part 
of the nerve supplies the sterno-mastoid and trapezius muscles. Some 
of the cervical nerves assist in partially innervating these muscles so 
that paralysis of the eleventh nerve does not eventuate always in the 
complete destruction of their function. The control of the sterno- 
mastoid is almost completely a function of the eleventh nerve. The 



THE NON-NEURONIC DISEASES 66l 

trapezius is in its clavicular portion quite a little subject to the acces- 
sorius nerve. 

Disease of the cervical cord and spinal roots may affect the nerve. 
Also is it liable to damage from carious vertebra?, here, from exostoses, 
abscesses, tuberculous and syphilitic conditions, tumors and menin- 
gitic exudations. Compression may occur from trouble in the fora- 
men magnum. The nerve may be primarily inflamed and this neuritis 
may be unilateral or bilateral. 

The chief symptoms of disease in this nerve are complete paraly- 
sis of the sterno-mastoid muscle, partial paralysis in the trapezius. The 
latter does not produce much of a deformity. The former causes one 
form of torticollis or wryneck. The chin cannot be moved back towards 
the side of the diseased muscle. When both sterno-mastoids are 
affected, the head falls back upon the shoulders. 

Prognosis and treatment need no special comment as they follow 
the ordinary principles for peripheral neuritic disease. 

THE HYPOGLOSSAL, OR TWELFTH CRANIAL NERVE. 

This is a pure motor nerve ; springs from a nucleus in the medulla 
that corresponds with the upward extension of the anterior horn of the 
cord ; and in some of the lower animals is a pure spinal nerve. It ap- 
pears at the side of the medulla between the pyramid and olivary body. 
It supplies, alone or in conjunction with branches from some spinal 
nerves, all the muscles connected with the hyoid bone, including the 
tongue, but excepting the digastric, stylo-hyoid, mylo-hyoid and the 
middle constrictor of the pharynx. It stimulates also the sterno-thyroid 
muscle. It is in connection with the pneumogastric, lingual, upper 
three cervical nerves, and the sympathetic. 

The nerve is more often damaged within its cerebral and medullary 
course than outside. It occurs in association with cerebral hemiplegia, 
the tract connecting the cortical center for the tongue with the hypo- 
glossal nucleus in the medulla running along through the internal cap- 
sule and crus with the tract for the extremities. In this hemiplegic 
form of the parlysis, of couse, there is no muscular atrophy. 

Bilateral or unilateral atrophic paralysis of the tongue is usually 
a medulla disease. 

Peripheral damage to the nerve may be caused by favorably 
located tumors, meningitic exudations, 'hone disease, basal hemorrhage, 
aneurisms of the verebral artery and dislocations of the upper cervical 
vertebrae. It has accompanied hydatid cysts. Cervical traumata and 
tumors may injuriously compress the nerve. Rarely there may be an 
isolated neuritis, following an infection of some sort, such as scarlatina. 

It may be associated with tabes, disseminated sclerosis, syringo- 
myelia, facial hemiatrophy and disease of other cranial nerves. 

If the palsy is bilateral the tongue lies dead and limp Otl the floor 
of the mouth. If it is unilateral the tip <>| the- tongue inclines toward 
the normal side but upon protrusion of it, the whole tongue moves 
toward the paralyzed side. The root of the tongue, according to 
Gowers, is a little higher on the paralyzed than on the sound side. The 









662 



THE NON-NEURONIC DISEASES 



raphe is arched, with the concavity toward the paralyzed side. The 
deviation is one of the results of the atrophy in the genioglossus 
muscle. 

This paralysis, like all neuritic peripheral palsies, is accompanied 
by muscular atrophy, flaccidity, fibrillary tremor, incomplete reaction 
of degeneration and reflex alteration. 

The speech, mastication, deglutition are not very much embar- 
rassed when the palsy is unilateral. When it is bilateral they may be 
very markedly disturbed, such trouble being usually of medullary 
origin. 

The prognosis is favorable in syphilitic, traumatic and rheumatic 
cases. Other cases are relatively unfavorable. 

The treatment should be carried out along the lines indicated un- 
der the head of neuritis and the other cranial nerves. 



PART in 



Non-Neuronic Diseases of the Brain. 



ANATOMY AND PHYSIOLOGY OF THE BRAIN. CERE- 
BRAL LOCALIZATION. CRANIO-CEREBRAL TOPOG- 
RAPHY. SYMPTOMS OF DISEASE OF THE BRAIN. 




Anatomy. — As I have shown under the head of the anatomy of 
the spinal cord, it is unfortunate that the gross and artificial division 
of the cerebrospinal axis into the brain and cord has become so estab- 
lished in the minds of the profession. It is not a physiological divis- 
ion and for the proper conception of nervous diseases, the physiology 
of the nervous system is a matter of infinitely greater importance than 
is its mere anatomy. I am convinced that much of the commonly ex- 
pressed difficulty in the understanding of nervous diseases, is due to 
the fact that anatomy and physiology have not hitherto taught the 
structure of the nervous system in the same way. The former has 
used, and unfortunately still uses, coarse, artificial lines of division, a 
misleading nomenclature and an irrelevant method of description. The 
student has always to revise his* anatomical lore as soon as he begins 
to delve into the physiology of the nervous system. If he is lucky in 
forgetting much of his anatomy and relearning it upon a physiological 
basis, he will have no trouble in understanding the diseases of the 
nervous system. If, however, he is a busy practitioner, who acquired 
his anatomical knowledge long ago and who now has no time to fol- 
low up the latest physiological discoveries, he will not understand the 
diseases of the nervous system. lie will constantly find them a puzzle 
and a mystery. These diseases represent physiological and anatomico- 
physiological changes and not merely anatomical abnormalities. The 



THE NON-NEURONIC DISEASES 663 

onlv salvation for the old graduate is to forget his old anatomical 
studies and relearn the structure of the nervous system upon the mod- 
ern physiological basis. He must learn that cerebrum, medulla and 
cord, for instance, are not separate organs, having their own duties 
to perform ; for they all work together and in unison as one great 
organ. A still better way to put it would be that these names merely 
indicate a certain general locality in which are found some of the 
serial deposits of gray matter that make up the whole apparatus and 
from whose cells processes run back and forth from one to the other. 
The brain, so-called, consists merely of that particular set of ganglionic 
masses that happen to be inside of the skull. Neither anatomically nor 
functionally does the skull limit them, however. They are as much 
in touch with the cord, anatomically and physiologically, and the cord is 
as much in touch with them as one lobe of the liver is with another 
lobe of the liver. Nay, more, they are in closer touch than are the 
hepatic lobes, for cerebral elements actually reach down (pyramidal 
tracts) and become a part of the cord, and spinal elements (direct 
cerebellar tracts, for instance,) extend up and become parts of the 
brain. 

In using the old nomenclature and the old anatomical divisions and 
subdivisions of the nervous system, I do so in deference to the long- 
grounded conception of the nervous system still held throughout the 
profession, and because it would be too radical to all at once cease 
using convenient names simply because they happen to convey erro- 
neous physiological ideas. Some day we will speak everywhere and 
under all circumstances of the cerebrospinal axis as a single organ, 
just as we now do of the liver. There will grow up in our minds the 
truth that this is a composite organ with one universal function through- 
out all of its parts, just as is the case with the liver. We 
will realize that essentially the cells (neurones) of one part of this 
organ do not functionate per se differently from the cells (neurones) 
of another part. We will be reconciled to the startling fact that the 
apparent differences between the functions of these widely separated 
neurones or constituent cells of the cerebrospinal organ are due merely 
to the differences between the end-organs to which they respctively 
happen to be attached. Certain brain cells see, let us say, and the 
cord cells do not see, because the former are attached to a particularly 
differentiated end-organ of epiblastic origin, the eye, that is different 
from any end-organ with which the cord happens to be attached. The 
cells themselves, both anatomically and physiologically, however, are 
from all evidence, exactly the same. This fact must be kept well in 
mind in our studies of the physiology of the brain or any other part 
of the nervous system. 

With the understanding, therefore, that old names are used tor 
mere rough topographical purposes, and not in any sense as convey- 
ing a correct idea of the anatomico-ph\ siologieal structure of the nerv- 
ous system, as we now know it, I will take up the anatomy and phys- 
iology of the brain. 

The brain, or encephaioii, is all of that part of the nervous sys- 
tem that lies above the foramen magnum in the occipital bone and 



66 4 



THE NON-NEURONIC DISEASES 



which fills the great cranial cavity. Conventionally it is said to be 
attached to the spinal cord at the foramen magnum. It is a large, 
ovoid, convoluted mass, smooth and covered with membranes. Turn- 
ing it upside down we see that we can divide it conveniently, for 
topographical purposes, into four sub-masses ; the cerebrum, the cere- 
bellum, the pons Varolii, and the medulla oblongata. 

The weight of the brain is a matter of some importance. For the 
majority of males it ranges between 1,300 and 1,450 grammes. The 
female brain weighs a trifle less. The heaviest brain that has been 
put upon record was that of Bismarck. It was calculated to have 
weighed over 1,867 grammes. Brain weight not only varies in ac- 
cordance with the sex but with the intelligence, the age and the race 
as well. 

The question of the relationship between brain weight and intel- 
ligence has long been debated. Intelligence is an elastic term. There 
are men of a high degree of intelligence in one direction, but of dense 
ignorance in another. Both with or without cultivation, intelligence 
may mean something very different between two men. The only real 
standard of intelligence that we could adopt would be one that en- 
compassed all knowledge and all mentality. That is never seen and 
hence our definitions of intelligence are always partial. It is a fact 
that in a few instances of special lines of mental cultivation, correspond- 
ing parts of the brain have shown some special development. Gam- 
betta was a great orator. His speech center in the brain was said to 
have been uncommonly developed. The visual centers in the occipital 
lobe have been found well developed in artists. These suggestive facts 
taken in conjunction with the truth that men of marked intellectuality 
and that certain superior races have had heavier brains than others, one 
is almost inclined to believe that brain weight has a great deal to do 
with intelligence. Cuvier's brain weighed 1,830 grammes; Byron's, 
1,807; Kant's, 1,650; Schiller's, 1,630; and Dantes', 1,420. English, 
Scotch and German brains are heavier than those of the Russians, 
French and Italians. Some of the smallest brains found are among 
the primitive African and Australian races. The negro brain averages 
about 1,250 grammes. Perls and Edinger have worked at the prob- 
lem from another side and obtained similarly suggestive results. They 
noticed that many men of eminence in the intellectual sphere give 
evidence of having had hydrocephalus which had healed in childhood. 
Such was probably the case with Rubenstein, Cuvier, Walter Scott 
and others. It is suggested that this favored brain expansion with 
possible increase in weight and size. Of course, it is understood in 
this that mere bigness of brain does not create intelligence by any 
means. One of the finest and largest brains I ever removed at a post 
mortem was from a man who scarcely had his equal for ignorance and 
stupidity. It is inferred merely that largeness of brain furnishes a 
large capacity for intelligence if it is exercised. 

All brains that weigh less than 1,130 grammes in man, or 990 in 
woman, are spoken of as microcephalic ; all that weigh over 1,490 
in man, or 1,345 in woman, are referred to as megalocephalic. 

At birth the brain weighs about 327 grammes. Up to four years 






THE XOX-XEUROXIC DISEASES 



665 



of age it grows very rapidly. From four to seven, its growth is slower. 
From the latter age to twenty its increase in size is very slow. Then 
it remains stationary. At 45 and 50, in men and women respectively, 
it begins to lose in weight but very slowly. At eighty it has lost about 
120 grammes. The relation of the brain to the body development, of 
course, must be always taken into count. The relative weight is about 
2 per cent. 

The Membranes of the Brain. — There are three membranes that 
cover the brain, namely, the dura mater, the arachnoid, and the pia 
mater. 

The dura mater is an inelastic and dense structure, composed of 

FIGURE 145. 




rUxu-t spinal, iut. 

The blood-vessels of the dura mater. Lateral view. (After Heitzmann.) 



white fibrous and yellow elastic tissue and is lined on its under sur- 
face with flat endothelial cells. It consists of two layers. The outer 
layer is the nutrient endosteum and is attached more tightly to the 
bones at the base of the skull than at the vertex. Through the cranial 
sutures and various foramina it becomes continuous with the perios- 
teum on the outside of the skull. 

The inner layer separates from the outer to form the sheaths of 
the cranial nerves and the great venous sinuses. Moreover it sends 
down between the main divisions of the brain the great septa called 
processes. 

The falx cerebri and the fcil.v ccrcbelli arc vertical curtains that 
hang in the great longitudinal fissure and separate the two halves of 
the brain. Another curtain is the tentorium ccrcbelli which passes 
horizontally forward into the transverse fissure and separates the pos- 
terior part of the cerebrum from the cerebellum. 



666 



THE NON-NEURONIC DISEASES 



The bony attachments of the falx cerebri are the crusta galli in 
front and the internal occipital protuberance behind. It is also fastened 
to the upper surface of the tentorium, along the occipital crest and to 
the posterior border of the foramen magnum. In the upper convex 
and lower free borders of this falx are the superior and inferior longi- 
tudinal sinuses, the superior extending from the foramen caecum back 
to the torcular Herophili at the internal occipital protuberance, and the 
inferior uniting with the common vein of Galen, or vena cerebri magna, 
and becoming the sinus rectus that courses through the tentorium to 
the torcular. 

The attachments of the falx cerebelli are the inferior surface of 

FIGURE 146. 




The blood- vessel* of the dura mater. Bird's-eye view. (After Heitzmann.) 

the tentorium and the occipital crest to the posterior edge of the fora- 
men magnum. Through this septum runs the occipital sinus or sinuses 
from the foramen magnum upwards and backwards to the torcular. 

The fastenings of the tentorium are the internal occipital pro- 
tuberance, the petrous bone and the clinoid processes of the sphenoid. 
Through a large notch the brain stem is transmitted. At its sides are 
the lateral sinuses. These run from the torcular, along the horizon- 
tal arms of the occipital crucial ridge to the petrous bone where the 
corresponding superior petrosal sinuses enter them and finally turn 
downward through the sigmoid fossa, uniting with the inferior petro- 
sal sinuses in the jugular foramina. 

The pituitary fossa is specially covered by a portion of the dura 
called the diaphragm selhe. 



THE NON-XEUROXIC DISEASES 667 

It will be observed that the various parts of the brain are by 
these dural septa encased in membranous boxes, as it were. This pro- 
tects the brain from sudden jars. It also limits and directs the course 
of hemorrhagic and purulent collections that may form in them or 
enter from without. 

In addition to the sinuses that have already been mentioned, notice 
must be taken of the circular sinus around the sella turcica, the two 
cavernous sinuses on either side and joined by the circular, and the 
.transverse or basilar sinus that unites the inferior petrosal sinuses. 

The dura receives its blood supply from the anterior and poste- 
rior ethmoidal branches of the ophthalmic, from the anterior menin- 
geal of the internal carotid, the great and small meningeals, from the 
internal maxillary, the meningeal branches of the ascending pharyngeal 
and occipital, and the posterior meningeal branch of the vertebral. The 
important artery is the middle meningeal from the external carotid. 

The veins are numerous and connect with those of the cranium. 

The dura is the only cerebral membrane that has a nerve supply. 
There are branches from the sympathetic that accompany the arteries. 
There are also branches from the trochlear, the ophthalmic, the Gasse- 
rian ganglion, and the tenth and twelfth. The motor branches of the 
nerves innervate the arteries. 

The arachnoid is a loose membrane, delicate and lace-like. The 
inner surface is so attached to the pia mater by trabecular that there 
are a lot of inter-communicating subarachnoidal spaces filled with cere- 
brospinal fluid. On the outer surface are the enlarged villi, known 
as Pacchionian bodies, or granulationes arachnoideales, that project 
within and along the superior longitudinal sinus and that probably 
serve as an outlet for the subarachnoid fluid into the sinus. The mem- 
brane follows the inner surface of the dura and does not dip into the 
sulci with the pia. The posterior subarachnoid space communicates 
with the fourth ventricle through the foramen of Magendie and the 
foramina of Key and Retzius. The arachnoid is without vessels and 
nerves. 

The pia mater is a highly vascular membrane consisting of a net- 
work of arteries and veins held together by fibro-elastic areolar tissue. 
Outwardly its epithelium lines the subarachnoid trabecular and spaces. 
These spaces are very large at the base of the brain. The pia hugs 
closely the surface of the brain and sends septa and bloodvessels vertic- 
ally into the brain substance. It dips down everywhere into the sulci 
and it forms investing sheaths to the cranial nerves. Between the 
fornix and the interbrain it enters the choroid fissure and ultimately 
becomes the velum interpositum and part of the tela choroidea ven- 
triculi tertii. Between the medulla and cerebellum it is inserted over 
the fourth ventricle and helps to form the posterior choroid tela which 
is perforated by the foramina of Magendie, Key and Retzius. 

The anterior, middle and posterior cerebral arteries, the anterior 
and posterior inferior cerebellar and the superior cerebellar all sup- 
ply the pia. Its venous supply is also abundant. The veins all empty 
into the sinuses and are the venae Galeni, choroid plexuses of tin- ven- 
tricles and the cerebral veins. The sympathetic, of course, innervates 



668 



THE NON-NEURONIC DISEASES 



it, as well as the third, fifth, sixth, seventh, ninth, tenth and eleventh 
cranial nerves. 

General Anatomy of the Brain. — A brief study of the embryo- 
logical development of the brain makes clear certain facts that it is 
well to understand before going on with a discussion of its anatomical 
structure. 

By the fifteenth day after conception, the neural tube resulting 
from the infolding of the epiblast, is complete, except for a short dis- 
tance posteriorly. In that portion which is to become the encephalon, 
or brain, later on, two constrictions take place which divide it into 

FIGURE 147. 

Epithalamus (Corpus pineale) Metathalamus (Corpora geniculate) 



Thalamus 



Sl^^NX Corpora quadrigemina 
efeficephalqr 

{ % 

Pedunculus cerebri 




Rhinencephalon 

Corpus striatum 
Sulcus hypothalamics [Monroi] , 
Hypothalamus * 
Chiasm* opticum 



Cerebellum 
Fossa rhomboidea 



Brain of the human embryo five weeks old. 
(After His.) 



Right half viewed from the lelt- 



three primary brain vesicles. Behind the third vesicle, the tube con- 
tinues small and constitutes the later spinal cord. The brain vesicles 
develop rapidly and again break up into subdivisions. A constriction 
appears in the anterior and posterior vesicles. Thus ultimately there 
are five vesicles. These with their surrounding elements are named 
from before backwards, the Prosencephalon, or Telencephalon ; the 
Thalamencephalon, or Diencephalon ; the Mesencephalon ; the Meten- 
cephalon ; and the Myelencephalon. 

As development goes on the various parts of the brain assume 
their adult appearance in these vesicular areas and the interconnected 
cavity within them becomes the ventricles. The adult ventricles consist 
of the two lateral, the third, fourth and fifth; with the foramina of 
Monroe connecting, y-shape, the two lateral with the third, and the 
aqueduct of Sylvius the third with the fourth. 



THE NON-NEURONIC DISEASES 



669 



Along the sides of these ventricles can be traced the groove or 
line of Monroe which, according to Minot, is of great significance in 

FIGURE 148. 




Embryonal Development of the Brain. 

A — Brain and Spinal Cord at the Third Month. 
B — Base of the Brain at the Fourth Month. 
C — Median surface of the Brain at the Fourth Month. 
D — Outer surface of a Cerebral Hemisphere at the Fifth Month. 
Jakob.) 



(After 



showing the developmental separation between the dorsal or receiving 
zone of the cerebrospinal organ and the ventral or emissive zone. In 






670 



THE NON-NEURONIC DISEASES 



the former are small nerve cells whose processes never pass out of the 
central nervous apparatus to form nerves. In the latter are the large 
cells whose processes do pass out to become nerves. The sensory 
nerve paths which are received by the dorsal zone are the processes 
of the cells in the cranial nerve ganglia and posterior spinal ganglia 
which are developed out of the original neural crests and not directly 
from that part of the neural tube from which the brain and cord de- 
velop. 

FIGURE 149. 



FRONTAL 10BE 




(After Gray.) 

The parts around the vesicles are not all equally elaborated in 
the adult brain. For instance, the prosencephelon in man becomes 
enormously developed into the cerebral cortex. The diencephalon is 
rather poorly developed and the olfactory projections (erroneously 
called nerves) are actually atrophied. In some lower animals the olfac- 
tory bulbs are larger than the cerebral hemispheres. The mesen- 
cephalon is a rudimentary organ. The metencephalon is well elabor- 
ated, whereas the myelencephalon is again relatively undeveloped. 

Three great flexures occur in the cephalic part of the neural tube, 
two ventral and one dorsal, which further help to disguise the primi- 



THE XOX-XEUROXIC DISEASES 



67I 



tive origin of the brain and cord of the adult. The mesencephalic 
ventral flexure is a very early one and at about the twenty-eighth day 
amounts to nearly 180 degrees. The thalamencephalon is thus brought 
almost into contact with the epencephalon. A cervical, ventral flexure 
occurs where the last vesicle joins the spinal cord. It represents the 
bending of the head upon the body of the embryo and at about the 
fourth week it amounts to 90 degrees. There is finally a late dorsal 
flexure, sometimes called the metencephalic, at the point where the 



FIGURE 150. 

View 
of the corpus 
callosum from 
above (from 
Sappey after Fo- 
ville). 4 

The upper sur- 
face of the corpus 
callosum has been 
fully exposed by 
separating the ce- 
rebral hemispheres 
and throwing them, 
to the side ; the gy- 
rus fornicatus has 
been partly de- 
tached, and the 
transverse fibres of 
the corpus callo- 
sum traced for 
some distance into 
the cerebral medul- 
lary substance. 

l,the upper sur- 
face of the corpus 
callosum ; 2, me- 
dian furrow or 
raphe ; 3, longitu- 
dinal striae bound- 
ing the furrow ; 
4, swelling formed 
by the transverse 

bands as they pass into the cerebrum, arching over the side of the lateral ventricle ; 5, 
anterior extremity or knee of the corpus callosum ; 6, posterior extremity ; 7, anterior, 
and 8, posterior fibres proceeding from the corpus callosum into the frontal and occipital 
lobes respectively ; 9, margin of the swelling ; 10, anterior part of the gyrus fornicatus ; 
11, fissure between the corpus callosum and this convolution opened out ; outside 12, is 
the termination of the calloso-niarginal fissure, and before 13 is the parieto-occipital 
fissure; 13, upper surface of the cerebellum 

fourth and fifth vesicles approximate. B3 the eighth week it amounts 
to 180 degrees and thus causes the dorsal part of the cerebellum to 
partially rest upon the medulla oblongata. The cervical and meten- 
cephalic flexures are temporary ; the mesencephalic is permanent. 

This is all the result of the working of the laws of evolution and 
in large part represents the principle of adaptation to environment. The 
value of this lies in the fact that we can thus unravel the complicated 
architecture and functions of the adult human brain by the compara- 
tive study of the lower and less developed brains of the animal world. 




6j2 THE NON-NEURONIC DISEASES 

The marvelous harmony and consistency of nature are thus not only 
realized in the primitive tracings of the highest expression of vital de- 
velopment, the human brain, but the value of all morphological and 
biological studies is enormously enhanced. 

I will now resume the general anatomical description of the en- 
cephalon. The following ganglionic deposits and their connecting pro- 
cesses are to be passed in review: 

I. Cerebrum (Prosencephalon) consisting of 

a. Hemispheres (Telencephalon), 

Their cortex and centrum ovale, 

Corpus callosum, 

Fornix, 

Commissura hippocampi, and 

Anterior commissure. 

b. Interbrain (Diencephalon), 
Lamina cinerea, 

Tuber cinereum and infundibulum, 
Pituitary body or hypophysis cerebri, 
Corpora albicantia, 
Optic thalami, 

Middle and posterior commissure, 
Pineal body or epiphysis cerebri, 
External geniculate bodies, 
Optic tracts and commissure. 

II. Midbrain, Crus Cerebri or Pedunculus Cerebri 
Crustae ( Mesencephalon ) , 

Substantia nigra, 

Tegmentum, 

Corpora quadrigemina, 

Internal geniculate bodies. 

III. Hindbrain (Metencephalon), 

Pons Varolii, 
Cerebellum. 

IV. Afterbrain (Myelencephalon), 

Medulla oblongata. 

Most of these parts are shown in the accompanying diagrams. For 
a further general anatomical description of them the reader is referred 
to works upon anatomy. 

Lobes, Convolutions, Fissures and Sulci of tlic Brain. — It is im- 
portant for topographical purposes that the surface of the brain be 
mapped out in areas and named. The fissures and sulci serve as most 
convenient lines of division. The accompanying maps of the brain 
will assist the reader and save a long description. 

The surface of the brain is called the cortex. It is seen to be 
divided into a great many subdivisions, as though it were made up of 
a mass of worms, by large and small fissures. The fissures are re- 
ferred to as primary and secondary. They represent infoldings of the 
cortex, allowing thus of a great area to be packed away in a small 






THE XOX-XEUROXIC DISEASES 



673 



space. This is a condition of comparative intelligence and evolution- 
ary development, for primitive brains are deficient in fissuration. The 
higher in the scale of life the animal is the greater the amount of 
convoluting is there of the brain surface. The fissures and sulci corre- 
spond with the developmental rearrangement, therefore, of various 
ganglionic deposits in the brain to accommodate them to the narrow 
capacity of the skull. This is virtually true of all of them, but as some 
of them seem to be older and more fundamental, more permanent, 



FIGURE 151. 

LobU9 irontalis 



Cavuni sei>ti pellucidi 
Lamina so^ii pellucidi 



Corpus callosum (cut through) 



Foramen interventricular* 

[Monroi| 



Columna fornici* 



Lobus temporalis 



Corpus fornicis 




Taenia former 



us striatum 
Caput nuclei caudati 
Capsr.la interna 

Nucleus leutiformis 
Stria terminate 



Hippocampus 



Pars centralis 
ventriculi 
lateralis 

Comu inferius 
ventriculi 
lateralis 



Cauda nuclei 

caudati 

Plexus chorioi- 

deus ventriculi 

lateralis 



Bulbus comu posteriori 



Cornu posterius ventriculi 
lateralis 



Fissura calcarina 

Lobus occipital! 



Spleniuni corporis callosi 



Lateral Ventricle, opened, viewed from above. 
(After Spalteholz.) 



than others, we speak of them as the primary fissures, and the others 
as the secondary. 

The primary fissures of the brain arc : 

The Longitudinal, between the two hemispheres. 

The Transverse, or choroidal, extending in betweeen the cerebrum 
and cerebellum. 

The Rolandic, on the upper mid-surface of the cerebrum. This 
is a most important localizing fissure from the surgical point of view. 






674 



THE NON-NEURONIC DISEASES 



The Sylvian, in the mid-lateral area, and important on account 
of the middle meningeal artery that passes up along it. 

The Parietooccipital, on the posterior internal surface of the 
hemisphere chiefly. 

The Calcarine and Parietal fissures are by some classified as pri- 
mary. 

Five great general divisions of the surface of the brain are out- 




Lobus temporalis 



Digitationea 
ippocampi 

Cornu infer I us 
ventriculi lateralis. 

Uncus 
fgyri bippo<:ampi] 
yTus hippocampi 
Eminent ia 
collaterals 
Fascia d^ctaja 
hippocampi 
Fimbria 
hippocampi 
Taenia fimbriae. 



Hippocampus 



Crus fornicis 



Trigonum collaterale 



Fissura calcari 



Trigonum habenulae 
Commissnra habenularuin 



Lobus occipitalis 



Third Ventricle, opened, viewed from above. 
(After Spalteholz.) 

lined by these fissures. Above the Sylvian and in front of the Rolan- 
dic fissure is the Frontal Lobe. Above the Sylvian and behind the 
Rolandic is the Parietal Lobe. Below the horizontal limb of the Syl- 
vian fissure lies the Temporal or Temporo-sphenoidal Lobe. Behind 
the Parietooccipital is the Occipital Lobe. If the Sylvian fissure be 
separated, a cortical area will be found lying at the bottom of it. This 
is the Central Lobe or Island of AY/7, and contains the great central 
ganglia. To these are sometimes added the Limbic Lobe, on the mesial 
surface of the hemisphere just above the corpus callosum, and the 
Olfactory Lobe or Bulb which is so much atrophied in man. 



THE XOX- NEURONIC DISEASES 



675 



These lobes are again subdivided into lobules and convolutions by 
the secondary fissures and sulci. 

On the outer surface of the Frontal Lobe are two horizontal and 
one vertical sulcus, thus forming a superior, middle and inferior con- 
volution, and behind them the precentral or ascending central convolu- 
tion. The part of the lobe that is immediately behind the short, ver- 

FIGURE 153. 




Schematic representation of the cerebrum viewed from ab 



tical limb of the Sylvian fissure is known as the operculum. The mesial 
surface of the lobe includes the paracentral lobule, just in front of the 
posterior end of the calloso-marginal fissure, and the superior frontal 
gyrus in front of that. The basal surface is grooved for the olfactory 
bulb. 

The Parietal Lobe includes on the outer surface the postcentral 



676 



THE NON-NEURONIC DISEASES 



or posterior ascending convolution and the upper and lower lobules, 
separated by the interparietal sulcus, which is long, arched and fre- 
quently interrupted. The convolution of the inferior lobule that sur- 
rounds the posterior end of the horizontal limb of the fissure of Syl- 
vius is known as the supra-marginal. That which surrounds the pos- 
terior end in like manner of the superior temporal fissure is called the 
angular gyrus. The forward end of the interparietal fissure is the 
inferior retrocentral, and the hinder end the anterior occipital. So im- 
portant are the ascending convolutions on either side of the fissure of 
Rolando, that we are beginning to put them together and call them 
the central lobule. This must not be confounded with the central lobe, 
or Island of Reil. On the median surface of the hemisphere the parietal 

FIGURE 154- 




Schematic representation of the right cerebral hemisphere. 



lobe runs over into the precuneus just above the parieto-occipital fis- 
sure. The precuneus is continued forward as the gyrus fornkatus, 
which lies just above the corpus callosum and curves around the knee 
in front, to terminate in the subcallossal gyrus. Above the fornicate 
gyrus is the c alio so -marginal sulcus. 

On the exterior surface of the Occipital Lobe we find the supe- 
rior, middle and inferior gyri, the first being separated from the 
parietal lobe by the anterior occipital sulcus and from the second occip- 
ital convolution by the lateral occipital sulcus. ( )n the median sur- 
face the cuncus is an important lobule, wedge-shaped, and lying be- 
tween the parieto-occipital above and the calcarine fissure below. On 
the under surface of this lobe is the end of the gyrus hippocampi, 
separated from the occipito-temporal gyrus by the occipitotemporal 
fissure. The gyrus hippocampi also appears on the median surface of 



THE XON-NEUROXIC DISEASES 



677 



the hemisphere just beneath the dentate gyrus and is continued back- 
ward into the lingual gyrus. 

The Temporal Lobe is divided into superior, middle and 
inferior convolutions by superior and inferior temporal sulci. 
On the mesial surface of the brain the middle tem- 
poral gyrus seems to run back into the gyrus fusiformis. The front 
part of the temporal lobe on the median surface is known as the uncus, 
or gyrus uncinatus. 

CRAXIO-CEREBRAL TOPOGRAPHY. 

For the guidance, of the surgeon, it is obviously necessary that 
the relationship of the underlying fissures and convolutions of the 

FIGURE 155. 




Schematic representation of the right cerebral hemisphere, viewed from the 



left. 



brain to the various parts of the outside of the skull shouM be known. 
l>roca, long ago, attempted to determine this by boring small holes 
through the skull, inserting pegs, then carefully removing the calva- 
rium and noting the parts of the brain that were damaged. Turner 
adopted the method of removing small parts of the bone and observ- 
ing the fissures and convolutions that appeared below. To Hefftler 
and Bischoff, Fere, Seguin and others are we indebted for very ac- 
curate knowledge as to this relationship between the brain and the 
sutures and other points on the skull. 

The fissures that it is especially desirable to know about in this 
respect are the Rolandic. Sylvian and Parieto-occipital. The accom- 
panying diagram shows the relationship. 

For surgical purposes, however, the marks on the skull are not 
always pronounced enough to serve as guides, hence other methods 



678 



THE XOX-NEURONIC DISEASES 



have been devised by Thane, Seguin, Horsley, Dana, Reid and Fraser. 
These methods are based upon exact measures, here and there, from 
definite and fixed points of prominence. 

All one needs is a steel, pliable tape measure and a blue pencil 
or brush with iodine on it. The head, of course, must be shaved. The 
innumerable instruments like the cyrtometer, encephalometer, may be 
dispensed with. 

FIGURE 156. 




Schematic representation of the base of the cerebrum. 

To locate the fissure of Rolando, the distance from the glabella 
to the inion has to be measured. About two centimeters behind the 
middle point on this line, or more accurately 55./ per cent, of the 
whole line measured back from the glabella, will be found the upper 
end of the fissure. In adult men this point generall) measures about 
48 mm. behind the bregma, in women 45, and in children from 30 to 
42, according to age. A line running downward and forward, at an 
angle of 67 degrees with the sagittal lino, will correspond with the 
tipper two-thirds of the fissure. The lower third is a trifle more vertical. 



THE XOX-XEUROXIC DISEASES 



6/9 



The end of the fissure below will just about touch a line drawn from 
the stephanion to the asterion. 

Bennet and Godlee's method for determining the Rolandic fissure 
is somewhat different and is based upon the views of Reid, largely. A 
vertical line is erected from the anterior border of the external audi- 
tory meatus. Measuring about two inches back of the point where 
this line cuts the glabella-inion-sagittal line, a parallel line is drawn 
vertically downward again and beside the posterior border of the 

FIGURE 157. 




Outline sketch op the skull, with the position of some of the 
principal cerebral sulci marked upon it £ 

Sy, Sylvian fissure; Sy.a., Sy.p., its anterior and posterior limbs ; /.J?., furrow of 
Rolando ; tr.fr. f., transverse frontal furrow ; i.par.f., intraparietal furrow; p.o., position 
of the parieto-occipital fissure; par.j. parallel furrow; m.t.s.f., middle temporo- 
sphenoidal furrow. 

( Modified from Thane. ) 

mastoid process. Where the posterior line touches the sagittal the 
upper end of the fissure is found. Its lower end corresponds with a 
point on the anterior vertical line about two inches above the upper 
border of the external auditory meatus. 

After the Rolandic fissure has thus been determined, it is an easy 
matter to establish the relative position of the central convolutions and 
their particular motor areas. 

The fissure of Sylvius, running horizontally, lies usually just a 
little above the parieto-squamous suture. A line following the external 
orbital process, the parieto-squamous suture and the parietal 
eminence will pretty nearly outline its course. The fissure is higher 
up and more oblique in children. The point of union between the ver- 



68o 



THE NON-NEURONIC DISEASES 



tical and horizontal limbs of this fissure is, according to Merkel, about 
four or four and a half centimeters above the middle of the zygomatic 
arch. 

The parieto-occipital fissure is determined by first finding the 
lambda, marking a point 3 mm. in front of it, drawing a line at right 
angles to the sagittal through this point, and then measuring about 
2.5 cm. on this line either side of the sagittal point. 

The frontal lobe lies almost entirely behind the frontal bone. 

Behind the parietal will be found the central convolutions 
the parietal lobe and a part of the occipital lobe. The parietal boss con- 
ceals the supra-marginal gyrus. The greater part of the temporal lobe 
is behind the temporal bone. 

Ofttimes it is desired to reach the ventricles. Usually there are 
several ways of doing this. Keen recommends the lateral route. 
Draw a base line through the lower border of the orbit and the ex- 
ternal auditory meatus. At a point on this line Ij4 inches behind the 
meatus erect a vertical line. A point on this vertical line \]/\ inches 
above the base line is where the trocar may be introduced. The in- 
strument should be plunged, after trephining, of course, into the brain 
in the direction of a point 2^ or 3 inches vertically above the oppo- 
site external auditory meatus. From 2 to 2V4 inches in the ventricle 
will be penetrated. 

The Minute Structure of the Brain. — I have enumerated the 
main anatomical parts of the brain. It is now necessary to discuss 
its minute structure. Like all other parts of the nervous system, this 
consists of a network of neurones, supported by sustentacular tissue 
consisting of neuroglia, connective tissue, bloodvessels, lymphatics and 
ependymal epithelium. 

The brain differs from the cord not in the character of its ele- 
ments but merely in the arrangement of them and the relative quantity 
of gray to white matter. The neurones are the same kind of neu- 
rones ; are bunched together in the same way ; have various sized 
processes ; and are distributed in relation to one another in contiguous 
series in the same way. It hardly needs to be said that the susten- 
tacular elements are exactly the same as those found outside of the 
cranium. It is obvious, therefore, that little need be said upon the 
constituent elements of the brain beyond what has already been said 
in the chapters devoted to the neurone and the neuronic architecture. 
Some consideration must be given, however, to the arrangement of 
these constituent elements in the encephalic mass. 

As in the cord, so here we find gray and white matter. The gray 
matter is spread out on the surface in the form of the cortex and de- 
posited here and there in clumps or bilateral masses all through the en- 
cephalon. The white matter appears in a large area just beneath the 
cortex and in streaks and radii here and there between the masses of 
gray matter, and between the brain and the parts of the nervous sys- 
tem outside of the head. It is very clear then that we have ganglia 
here, just as we have in the cord, consisting of little accumulations of 
neurone bodies in special spots and bundles of neuraxones making 
up the pathways along which impulses of all sorts travel between dif- 



THE XOX-XEURONIC DISEASES 



681 



ferent parts of the brain and between the brain and the rest of the 
nervous system. 

At a first glance we discover that the brain contains the following" 
deposits of gray matter or ganglionic collections of cells — viz., cerebral 
cortex, corpora striata, olfactory lobes, optic thalami, corpora genicu- 
lata, corpora albicantia, Luy's body, corpora quadrigemina, red nuclei, 
substantia nigra, cerebellar cortex, cerebellar nuclei, pontile nuclei, 
olivary bodies, nodal nuclei and the cranial nuclei. 

The processes of the cell bodies which enter into the composition 
of these ganglionic masses make up three great groups of tracts which 

FIGURE 158. 




Diagram to illustrate the association, 
the brain. 



'OmmtSSUral, and project ion tracts of 



constitute the white matter. They are the association tracts, the 
commissural tracts and the projection tracts. 

It now behooves us to analyze these ganglia and tracts a little more 
in detail. I would again urge the reader to note the great similarity, so 
far in our account, of the brain with the spinal cord. 

Cortex. — If the much infolded cerebral cortex were spread out 
smooth, as you would smooth out a handkerchief, it would be a thin 
sheet of gray matter, with an area of about three hundred square inches, 
and a fairly uniform thickness of about one-tenth or one-twelfth of an 
inch. Therefore the convolutions, which, by the way, correspond at 
the seventh month with those of the adult baboon, are seen, when the 



682 



THE NON-NEURONIC DISEASES 



brain is sliced transversely, to have a narrow gray border following 
all of their changes and detours. Running through the middle of this 
gray border, parallel to its edges, is a fine white line. In the vicinity of 







FIGURE 159. 






*■■ ■ 

m 



8! Kit .1 '',-"■, 'k|> i-.',.|. " 

■, ■''$•■ f'^ I ■''■■ ■■•".■"•■^v>"-: 




HUMAN CEREBRAL CORTEX. 

Central convolution. A, medullary substance; b, layer of swindle cells; c, radial bundles; 

d, giant pyramidal cells; e, large pyramidal cells; f, stratum of Baillarger; g, small 

pyramidal cells; h, tangential fibres; i, pia mater. 
Occipital lobe. A, medullary substance; b, layer of spindle cells; c, inner granular 

layer; d, layer of large pyramidal cells; e, miter granular layer: f, layer of Vici) 

d'Azyr; g, small pyramidal c Us; h. tangential film s. 
Conni ammonis. A, ependyma of lateral ventricle; b, medullary layer of alveus; c. 

layer of spindle cells; d. large pyramidal cells; e, stratum radiatum; f, layer of 

lacunae; g, small pyramidal cells; h, tangential fibres. 
Fascia dentata Tarini. A, spindle cells and nerve-fibres; b, large pyramidal cells; c, stra- 
tum granulosum (small pyramidal cells). 

(After llenda.) 



the calcarine fissure it is so distinct that it can be seen with the naked 
eye. It is here spoken of as the white line of Vicq d'Azyr. Under the 
microscope, here and in other convolutions, a second inner and finer 



THE NON-NEURONIC DISEASES 683 

line can be seen. It is known as the inner line of Baillarger. These 
lines at once demonstrate to us that the cortical gray substance is ar- 
ranged in layers. With a high power of the microscope it is observed 
that the gray lines represent the massing of cell-bodies, whereas the 
white striae are caused by the predominence of their processes. Five 
or seven different layers of cells have thus been differentiated in the 
cortex, and the effort is being made to assign to them respectively par- 
ticular functions. At the edge of the cortex, just beneath the pia mater, 
is a layer of neuroglia with only a few small neuronic cells in it. A 
great mass of fibres run through it parallel with the surface, for which 
reason they are spoken of as the tangential fibres. Just below the tan- 
gential fibres are the stria of Bechterew and Kaes. 

Xext below this come the small pyramidal cells, making up the 
ambiguous layer of Andriezen and the second general layer, counting 
the layer of tangential fibres as the first. The striae of Bechterew and 
Kaes make up the upper half of the second or ambiguous layer. Nu- 
merous small round cells mingle with the small pyramidal cells of this 
layer. 

Between the second and the third layers there is a superradiary 
network. The third layer is a very broad one, presents in its middle 
the appearance known as the striae of Baillarger, and is commonly called 
the large pyramidal cell layer. These cells are the largest in the 
cerebral cortex, are most abundant in the Rolandic area, and being 
triangular or pyramidal in shape, have their apices pointing in the 
direction of the tangential layer and send off from their bases great 
long neuraxones which run to the lowest depths of the cortex and out 
into the underlying white substance. From the apices project upwards 
long dendrites and from the sides shorter dendrites. The cells increase 
in size as we proceed downward in this layer, until we meet with the 
very largest of them at the bottom. Between this large pyramidal 
layer and the next, or fourth layer is an interradiary network. 

In the upper part of the fourth layer the cells suddenly appear 
small and spindle-shaped and hence the layer has been spoken of as the 
spindle cell layer, or layer of polymorphous cells. The lower part of 
this layer assumes a markedly fibrous appearance and has been recog- 
nized as being made up of Meynert's intra-cortical association fibres. 

Immediately beneath the last and fourth layer comes the white 
substance of the brain, made up largely here of the subcortical as 
ciation fibres. 

To recapitulate, then, the cerebral cortex from without inward is 
seen to be made up of the four great layers, the tangential, the small 
pyramidal, the large pyramidal and the spindle-celled. The other layers 
mentioned are mere subdivisions of these. Neurones and sustentacular 
tissue are the constituents. Nothing need be said further of these than 
what has already been mentioned. 

The large cells seem to be emissive or motor in function and are 
most abundant in the motor areas ; the small cells are probably receptive 
OT sensory and are found more numerous in the sensor) areas. This. 
of course, produces variations of a secondary sort in the appearance 
of the cortex. It is well, however, to keep in mind its more or I 



68 4 



THE NON-NEUROXIC DISEASES 

FIGURE 160. 




Tangential fibres. 



Stria? of Bechterew and de> 
Kaes. 



Superradiary network (of the. 
/ second and third layers). 



Striae of Baillarger. 



Interradiary network Cof tho 
third and fourth layers). 



Meynert's infracortical 
association fibres. 



Subcortical association 
fibres. 



Ram C o , r y 1 ci < ja;' i ; gram ° f tHe diffCm,t byerS ° f "" nnbni a "'" ^ After 



THE NON-NEURONIC DISEASES 685 

uniform four-layer appearance and not to confuse one's self with too 
fine a secondary subdivision of it. The directions in which the cells 
lie, their shapes and the minute course of their processes are morpho- 
logical facts that as yet have no special clinical significance. 

The primary fissures in the cerebral cortex average a little less 
than an inch (20 to 23 mm.) in depth. The total area of the cortex, 
according to Donaldson's careful estimation, is 2,352 sq. cm. Of this 
the frontal lobe has 41 per cent.; the parietal 21 per cent.; the tem- 
poral 27 per cent. ; the occipital 10 per cent. ; and the island of Reil 
1 per cent. It is roughly estimated that the total area of gray matter 
in the sulci is about twice that on the surface. After correcting, by 
recent data, the errors of judgment of Hammaberg, Meynert, Wagner 
and Donaldson, and supplying what they had obviously omitted, 
Thompson has estimated the number of cells in the cortex to be 9200 
millions. This is about 0.23 per cent, of the number of cells, by 
Francke's estimation, in the whole human body. This is undoubtedly 
the most accurate calculation of these marvelous elements that has 
ever been made. This enormous number of functional nerve cells 
makes up only 1.37 per cent, of the total volume of the cortex. 

These cells vary considerably in size. The small pyramidal and 
spinal cells measure from 1-1200 to 1-600 of an inch. There are many 
small round cells no larger than 1-2500 in. In the central and para- 
central convolutions may be seen the huge giant cells of Betz, which 
attain the size of 1-500 to 1-200 in. in diameter. These various types 
of cells are believed to have distinctive functions. In the second and 
granule layers are the small receiving cells. 

The spindle cells and cells of Cajal, nestling partly in the first and 
partly in the fourth layer, are believed to be associative and coordinat- 
ing in function. The large pyramidal cells in the third layer are almost 
certainly emissive cells. They resemble the large motor cells in the 
anterior horns of the cord. They are seen most abundantly in the 
motor areas of the cortex, whereas the smaller cells predominate in the 
sensory areas. A curious feature of these large, deeply-seated, pyra- 
midal cells is that their dendrites extend upwards a long distance and 
end in the tangential layer in dense, profuse ramifications. From these 
small, terminal branches a series of minute secondary twigs, each end- 
ing in a little knob, project laterally. The opportunity is thus afforded 
for countless possible combinations between the dendrites of the cells, 
such as a speculative psychologist would have never dared to imagine. 

The fibres of the cortex I have already indicated as the tangential 
and the striae of Uaillarger and the striae of Bechterew and kaes. To 
these should be added the superradiary, the interradiary layers and the 
intercortical and subcortical association fibres. They of course are all 
neuraxones from their respective cells. There are transverse or rather 
vertical fibres that come in from the sensory projection system and 
carry afferent impulses or pass out and carry efferent impulses. The 
association fibres are both long and short and represent the proa 
of the cells reaching over to arlx>rize around the cells in the next con- 
volution or more remote parts of the cortex. The short fibres pass 
around under the fissures, while the long run in all imaginable direc- 






686 






THE NON-NEURONIC DISEASES 



tions through the white centrum semiovale. The projection processes 
that pass in and out of the cortex are arranged in little bundles in such 
a way as to give the latter a columnar appearance. 

Olfactory Lobes. — These are parts of the brain and in structure 



FIGURE 161. 




. — Section across the hippocampus major, dentate fissure, dentate fascia 
and fimbria (after Henle). 

Gh, part of the gyms hippocampi or uncinate convolution : Fd, fascia dentata or 

flentate convolution ; between them is the dentate fissure ; Fi, fimbria, composed of 
ongitudinal fibres here cut across ; 1, 2, medullary centre of the hippocampal gyrus pro- 
longed around the hippocampus, H, as the so-called alveus, into the fimbria ; 3, layer of 
large pyramidal cells ; 4, stratum radiatum ; 5, stratum laciniosnm ; 6, superficial 
medullary lamina, involuted around the dentate fissure ; **, termination of this lamina, 
the fibres here running longitudinally; 7, superficial neuroglia, of the fascia dentata; 
*, stratum granulosum. 

reveal the typical cortical arrangement of the neurones. They have 
been termed the rhinencephalon and are developed from a secondary 
division of the first cerebral vesicle. The olfactory apparatus is a much 
atrophied affair in man. It includes, when traced from before back- 



THE XOX-XEUROXIC DISEASES 



687 



wards, the olfactory bulb with its peripheral processes, the olfactory 
tracts and their lateral roots, with the gray root or trigonum between 
them, the hippocampal convolution, cornua ammonis, part of the con- 
volution of the corpus callosum, the nerves of Lancisi and the anterior 
commissure. In addition to all this there are connections between the 
olfactory apparatus and the interbrain. 

FIGURE 162. 




Cortex of the olfactory bull) of the rabbit, showing tin- olfactory fibres, the 
stratum glomerulosum, the bipolar granule-cells, the layer of large' pyramidal 
eel'-, the externa; granular layer, the radial fibres, the internal granular layer and 
the medullary layer, from above downwards. (After Benda.) 



The medulla olfactorius, constituting the olfactory field, arises 
for the most part from the bulbu s. One tract, the olfactory bundle to 
the cornua ammonis .has been outlined. Another tract from tin- olfac- 
tory field runs backward and cm be followed into the region of the 
corpora albicmtia. It passes through the ventral regions of the Cor- 
pora striat'i. bnt receives no fibres from them. Some of these fibres 



688 



THE NON-NEURONIC DISEASES 



even go so far back as the region of the interpeduncular ganglia, per- 
haps even into the fillet. 

A third tract starts from the lateral parts of the medulla olfac- 
torius of the olfactory field and passes through the anterior part of 
the thalami. It then reaches the inner surface of the ventricle and as 
the taeniae thalami ultimately reaches the ganglia habenulae. Thus as 
a large complex of ganglia and bundles, running through the greater 
part of the brain, the olfactory fibres are to be traced as far as into the 
cerebral cortex on the one hand, and as far as the ganglion habenulae, 
and possibly the corpus mamillare, on the other. Other ganglia of the 
midbrain and interbrain stand in close connection with these ganglia. 

What are called the olfactory nerves are the central processes of 

FIGURE 163. 




—Nervous mechanism of the olfactory apparatus, a, bipolar cells of the olfactory 
apparatus (Max Schultze's olfactorial cejte) ; b, olfactory glomeruli ; c, mitral cells ; 
d, granule of white layer ; e, external root of the olfactory tract ; f, grey matter of 
the sphenoidal region of the cortex ; a, small cell of the mitral layer ; b, basket of a 
glomerulus ; c, spiny basket of a granule ; e, collateral of the axis-cylinder process of 
a mitral cell ; /, collaterals terminating in the molecular layer of the frontal and 
sphenoidal convolutions ; g, superficial triangular cells of the cortex : h, supporting 
epithelium cells of the olfactory mucous membrane. (Ramon y Cajal.) 

the sense cells of the olfactory mucous membrane in the nose. Passing 
through the cribriform plate, these processes decussate repeatedly after 
arriving at the ventral surface of the bulb. The arborization of each 
process intermingles with the thick branches of a dendritic process from 
a cell above and thus forms the complex roundish olfactory glomerulus. 
The cell above gives oft other processes of like nature, but only this one 
enters into relation with the peripheral cell in the glomerulus. Thus 
the pathway of smell impulses is seen to consist of a peripheral or pri- 
mary neurone and a central or secondary neurone. Other cells have 
been seen, however, in the cortex of the olfactory bulb, but their nature 
is still somewhat doubtful. These types of granular cells, marked a. b, 
c, are observed in the accompanying figure lying between the cells first 
described and the layer of medullated fibres. 

It will be observed that this illustration of the cortex of the bulb 
bears a most striking resemblance, upside down, to the cortex of the 
cerebrum. The layer of mitral cells, called so on account of their 



THE XOX-XEUROXIC DISEASES 



689 



shape, send up their neuraxones to become part of the olfactory tract. 
The granular cells have no axis cylinders, resemble the spongioblast 
cells of the retina and are merely associative in function. The neu- 
raxones of the olfactory tract have been traced, as described above, into 
the olfactory field of the brain. 

Corpora Striata. — These are two important basal ganglia which, 
with the optic thalami, are second only to the cortex. They not only 
modify impulses that pass through them, but they probably originate 

FIGURE 164. 



Lobus frontali! 



Commissar* anterior 
Pars tecta colomnae (omicis 

Caput nuclei caudati 



Pars frontalis capsulae internae 
Putanien 



Globus pallid 



Truncus corporis callosi 

Comu anterius rentriculi lateralii 
/ Caput nuclei caudati 

Pars libera colomnae forni 




Fasciculus 

[Vicq d'Aij-ii, 
Nucleus hrpothalamicus 
[Corpus LutsI' 
Para occipitalis 
capsulac interna*^ 
Fasciculus retro^ 
flexua [Meynerti; 

Nucleus ruber 
tegmenli "~ 
Stratum grLseum 
centrale — 

Corpus g*Dl- 

-coUtuiD mediate 



Lobus occioiial 



■na longltudinalis lateralis 

Horizontal section through the brain, viewed from above. In the left half of 
the picture, the plane of section is about 1 cm deeper than it is in the right half. 
(After Spalteholz.) 



subconscious impulses that play an important role 
Each striate body is divided into a caudate nucleus 
nucleus. Between the two nuclei dorsally run the 
sensory and motor pathways to and from the cortex 
ternal capsule, wherein a great mass of fibres from 
parts of the cortex are closely brought together. To 
the corpus is the external capsule and beyond that a 
gray matter known as the claustrum. 



in mentalization. 

and a lenticular 

it projection 

. This is the in- 

widcly separated 

the outer sid 
long thin strip of 









690 



THE NON-NEUROXIC DISEASES 



The internal capsule is a part of the brain that the clinician must 
keep always clear in his memory. As so many functional systems con- 
verge here, a small lesion may cause a wide distribution of sympto- 
matic manifestations. The arrangement of the pathways through it is 
relatively constant, so that if the lesion be small enough to affect but 
one of them we could theoretically definitely localize it. Just behind 
the genu or knee of the internal capsule course the great motor or 
pyramidal tracts from the cortex to the cord. In front of these, and 
therefore at just about the knee, are the facial and hypoglossal fibres. 
Behind the pyramidal tracts, in what is called the tegmental radiation, 
pass the sensory fibres with the pathway from the occipital to the 
beginning of the optic nerve most posteriorly. The other special sense 

FIGURE 165. 



Stria longitudinalis medial is 
Stria longitudinalis lateralis 
Truncus corporis callosi 

Cauda nuclei caudal 

Stria terminalis 

Vena terminalis 

Corpus fornicis 

Stratum zonale tbalami 

Lamina medullaris thalanii 

Nucleus anterior thalanii 

Nucleus lateralis thalanii 

Nucleus medialis thalanii 

Fasciculus thalamo- 

mamillaris [Vicq d'Azyri] 

Massa intermedia 

Capsula interna 

Nucleus lentiformis 

Hypothalamus 

Pedunculus cerebri 

Tractus opticus 



Sulcus corporis callos 
/ 




Lamina chorioidia 

epitheliaHs 

Pars centralis 

ventricuJi lateralis 

Plexus chorioideus 

ventriculi lateralis 

Ependyma ventriculi 

Lamina affix a 

Taenia cborioidea 



Taenia fornici 



Tela chorioidea 
ventriculi tertii 



Plexua chorioideus 

ventriculi tertii 
Taenia thalami 



'entriculus terliilS 



Nuclei corporis mamillaris' 

Frontal section through the middle of the third ventricle. (After Spalteholz.) 

paths are shown clinically as probably also passing through this part 
of the capsule. 

The caudate nucleus is anatomically divided into the head in front 
and the tail behind. The tail curves round the brain stem and can be 
traced almost to the inferior horn of the lateral ventricle. The head 
of the nucleus is related to the gray matter of the anterior perforated 
space. The nucleus is in continuation with the amygdalum of the 
cortex in the temporal lobe, the claustrum and the outer part of the 
lenticular nucleus. 

The lenticular nucleus is also in relation with the anterior per- 
forated space. It is significantly divided into the put amen, or outer 
portion, and the globus pallidus, or inner part. The putamen and 
caudate nucleus enter into the formation of the fibre system of the 
corpus striatum and thus constitute a rudimentary but biologically 
very ancient part of the central nervous system. By a few association 
fibres the corpus striatum is connected with the cortex above. By an 
abundant set of fibres which originate in its own cells it is brought 



THE XOX-XEUROXIC DISEASES 



69I 



into physiological association with various parts of its own substance 
and with parts below it. The cortical fibres that pass directly through 
it have been already referred to in the description of the internal cap- 
sule. The nucleus is in intimate connection with the corpus sub- 
thalamicum, optic thalamus, inferior olivary bodies and cerebellum and 
cranial nerve nuclei in the medulla. The putamen-caudate-nucleus is 
also in close union, by means of connecting fibres, with the globus palli- 
dus. The cells in this part of the brain measure from 1-1800 to 1-500 



FIGURE 166. 



1 rum us lorporis ( alio 
Septum ik.'11ii 
Pars centralis ventriculi lateral 
Caput nuclei t-andal 
Corpus fom 

Caaeola i 



Gyrus frontalis superior 

Bndiatio corporis eallosi 

Padialio corporis 



Capsola 




Corpus manitllare 



Foraiuon raeru 



Nucleus olivari« inferior 
I'vramis inedullae oblongatae 

Decussalio pyramid 



Vertical section through the brain, viewed from in front. In the left half of 
the cerebrum, a second cut was made parallel to the first and a plane presented to 
view somewhat farther dorsalward. (After Spalteholz.) 



in. in diameter. Some of them are very large and are found in the 
lenticular nucleus. 

Optic Thalami. — These are two large collections of nuclei that are 
on either side of the third ventricle. They are connected by the middle 
gray commissure. They form part of the walls of the lateral ventricles. 
As constituting the greater part of the interbrain, the thalami lie just 
behind the cerebrum. Their constituent nuclei are not sharply sep- 
arated from one another. They are referred to as the mesial, lateral 
and anterior nuclei. The pulvinar is the entire posterior part of the 
thalamus and, like a tumor, projects into the ventricle. ( )n the median 
border is the ganglion habenulce. Lying against the ventral and ex- 
ternal surface of the pulvinar and projecting far into its substance is 



692 



THE NON-NEURONIC DISEASES 



the peculiar grayish lateral geniculate body. It gives origin to many 
fibres of the optic tract. The thalamus is in connection with the corpus 
subthalamicum, the red nucleus and the corpora albicautia beneath it 
and with the geniculate bodies postero-external to it. The corpora 
quadrigemina are also in connection with it. 

The cells of the optic thalami are multipolar, rather large, and 
loosely grouped together. There is also a stellate, small cell. The 
associative Golgi type of cell is also found. The neuraxones from 
these cells pass up to the cortex. In it are also the terminal arboriza- 
tions of neuraxones of cells lying in the cortex above and in the sensory 
cranial and spinal nuclei below. The associative cells serve as the 
connecting links between these afferent and efferent paths that meet 
in the thalamus. Its anatomy indicates that this ganglion is a most 
important way station between a great mass of inpouring and out- 

FIGURE 167. 




— Scheme of the retinal elements. A, cones of the fovea centralis ; B, granules 
(nuclei) of these cones ; C, synapse between the cones and bipolar cells in external 
molecular layer ; D, synapse between the bipolar and ganglion cells in the internal 
molecular layer ; a and b, rods and cones in other regions of the retina ; c, bipolar cell 
destined for the cones ; d, bipolar cell destined for the rods ; E, e, ganglion cells ; 

{, spongioblast; g, efferent fibre (? trophic), originating from the cell m, in geniculate 
ody ; h, optic nerve ; i, terminal arborisations of optic nerve fibres in geniculate 
body ; /, fibre3 from the cells of geniculate body on the way to cerebral cortex. 
(B,. y Cajal.) 

going impulses. It is preeminently and first of all a great "receiving 
station" for fibres from the cortex and for fibres from the corpus 
striatum. In proportion to its great mass, it sends an exceeding small 
number of fibres downward. 

Optic Tracts. — As these are not nerves, but actual tracts of the 
brain, it will be appropriate to speak of them in this place. The retinal 
cells, like the olfactory cells and the spinal sensory cells in the posterior 
ganglia, send their central processes in to unite with the next set of 
lieu rones. 

The retina is a purely nervous structure and is made up of three 
layers, which are subdivided into six. The three primary layers are 
those of the visual cells, the bipolar cells and the ganglion cells. Each 
of these layers is divided into two again, as follows, layer of rods and 
cones and external granular layer, external molecular and internal 
granular layer, internal molecular and ganglionic layer. The neu- 
raxones of this last layer of cells become the optic tracts, each tract 
containing about 500,000 of them. The rods and cones are merely the 



THE XOX-XEUROXIC DISEASES 



693 



highly differentiated peripheral processes of the bipolar cells that make 
up the external granular layer. The central processes of these remark- 
able peripheral neurones pass inward to'come into apposition, by means 



FIGURE 168. 







^.^ X. 


\ l ^ = ~~ 


V- 




Y 


J : 




(-"MS A_L •' 


K MP0RA || 


V = 


===3 


^n 




*E 


^=< * 



'8U*' 



— Diagram of visual paths. (From Vialet, modified.) OP. N., Optic nerve. 
OP. C, Optic chiasm. OP. T.. Optic tract. OP. R., Optic radiations. GEN., Genic- 
ulate body. THO., Optic thalamus. C. QU., Corpora quadrigemina. C. C. Corpus 
callosum. V. S., Visual speech centre. A. S., Auditory speech centre. M. S„ Motor 
speech centre. A lesion at 1 causes blindness of that eye; at 2, bi-temporal hemia- 
nopia; at 3, nasal hemianopia. Symmetrical lesions at 3 and 3' would cause bi-nasal 
hemianopia; at 4, hemianopia of both eyes, with hemianopic pupillary inaction; at 
5 and 6, hemianopia of both eyes, pupillary reflexes normal ; at 7, amblyopia, espe- 
cially of opposite eye ; at 8, on left side, word-blindness. 

of their arborizations, with the second bipolar-cell layer, whos 

es have more or less of a horizontal direction. The ganglionic layer 
contains large horizontal cells, which are, according to Cajal, spon- 



694 



THE NON-NEURONIC DISEASES 



gioblasts. There are in the retina the terminal arborizations of cells 
embedded in the optic thalami, corpora geniculata and anterior corpora 
quadrigemina. These neurones, of course, carry the impulses from the 
primary optic centers to the retina, whereas the previous cells carry 
the impulses to the optic centers from the retina. 

The optic tracts partly decussate in the optic chiasm and then 
curve backwards around the crura to divide into the lateral and mesial 
root and ultimately terminate in arborizations in the primary optic 

FIGURE 169. 




— Section through the superior part cp one op the superior corpora 

QUADRIGEMINA AND THE ADJACENT PART OP THE OPTIC THALAMUS (after Meynert). 

5, aqueduct of Sylvius; gr, grey matter of the aqueduct; c.q.s, quadrigeminal 
eminence, consisting of : I, stratum le'mnisci ; 0, stratum opticum ; c, stratum cinereum ; 
Th, thalamus (pulvinar) ; c.g.i, c.g.e, intei-nal and external geniculate bodies ; br.s, 
br.i, superior and inferior brachia ; /, fillet; p.l, posterior longitudinal bundle; 
r, raphe ; III, third nerve ; n. Ill, its nucleus ; l.p.p, posterior perforated space ; 
s.n, substantia nigra ; above this is the tegmentum with its nucleus, the latter being 
indicated by the circular area ; cr, crusta ; II, optic tract : M, medullary centre of 
the hemisphere; n.c, nucleus caudatus; st, stria terminalis. 



centers — namely, the pulvinar, the external geniculate bodies and the 
anterior corpora quadrigemina. In the latter nuclei these optic fibres 
are brought into association with the oculomotor nerve, and thus is 
explained the reflexes of the eye. Moreover, these primary optic cen- 
ters are in connection with other cranial nerve nuclei in the medulla. 
The processes of the cells of these primary optic centers pass 
through the extreme posterior part of the internal capsule and c 
tinning on as the optic radiations of Gratiolet ultimately terminate in 
the cortex of the occipital lobe, chiefly the aniens. By reason of the 
partial decussation of the tract at the chiasm, the temporal half of each 
retina is connected with the occipital lobe of the same side, the nasal 
half with the lobe of the opposite side. This is shown in the accom- 



THE NOX-XEUROXIC DISEASES 



695 



panying diagram from Yialet. The fibres that connect the two tracts 
behind, running as a commissure between the primary nuclei, are not 
shown because they are of no significance clinically so far as we know. 

Regio Subthalamica. — This is a very complicated region just be- 
neath the optic thalami and contains a number of small grayish ganglia 
whose functions we do not know much about. The nucleus tegmenti, 
or red nucleus of the tegmentum, is highly vascular and rich in cells. 
External to this lies the lenticular-shaped Luys' body or corpus sub- 
thalamicum. It has a few cells, but rather abundant plexus of fibres. 

Somewhat mesial to Luys ? body is the substantia nigra of Somer- 
ing, an accumulation of grayish pigmented cells of rather large size. 
Dorsal to the substantia nigra is the tegmentum, or sensory part of the 

FIGURE 170. 







"TV o nrt o -T a nt i I e 

Transverse section through the corpora quadrigemina and cerebral peduncles ; 
diagrammatically represented, to show the relative positions of the prominent 
tracts. 

cerebral peduncles, while ventral to it is the pes or motor part con- 
taining the great fibre system of the motor cortex and capsule. A.S 
far as the end of the midbrain can the substantia nigra be demon- 
strated above the pes. In it terminates the last remnant of the fibre 
system from the corpus striatum. 

From the posterior part of the red nucleus a fibre system can be 
traced to the opposite half of the cerebellum. This is an important 
tract, the tr actus tegmento-cerebellaris. 

Corpora Quadrigemina. — These art- four tubercles just behind and 
l>eneath the optic thalami, two in front and two behind. Beneath them 
is the third ventricle and the upper end of the aqueduct of Sylvius. On 
top of them rests the epiphysis cerebri or pineal gland, which in some 
low forms of life has all the appearance of an atrophied primitive eye. 
It is sometimes called the conarium. It contains solid epithelial tubules, 



696 



THE NON-NEURONIC DISEASES 



an abundant blood-supply and the so-called brain-sand. This remark- 
able structure in several selachians and in many reptiles passes through 
a hole in the skull to a sense organ under the skin. In this organ we 
can see a cornea, a lens, a retina, and below this a pigmental layer. In 
the higher forms of life it has become useless and withdrawn into the 
head. 

Immediately in front of the pineal gland is the ganglion habenulce, 
which appears to receive fibres from the olfactory field by way of the 
tcenia thalami. 

From the anterior corpora quadrigemina arise part of the optic 
nerves. Thus we see three ganglia in this immediate neighborhood 

FIGURE 171. 



SJratum zonalc thalami 
Pulvinar 



Stratum griseum colliculi superior 
corporum quadrigeminorum 

Stratum zonale 



Corpus pineale 

Commissura posterior 
[cerebri] 

Stratum griseum tffi i 

centrale 
Aquaeductus 
cerebri [Sylvii] 
Forniatio reticularis 
(Nucleus lateralis superior) 
Nucleus n.oculomotorii- 
Fasciculus longitudi- 
nalis medialis 

Decussatio 
tegmenti dorsalis 



Nucleus ruber 
tegmenti 



Ganglion 
interpedunculare 




Capsula interna 

Corpus gcniculaturo 

mediate 
Lemniscus medialis 
[sensitivus] . 






Tractus opticus 



N. oculoqnotorius 



Pedunculus cerebri 



Substantia nigra 

Section at the level of the root of the oculomotorius nerve. (After Spalteholz.) 






serving as the origin of the optic nerves — namely, the pulvinar, the 
anterior corpora quadrigemina and the external geniculate bodies. 
They all receive fibres from the occipital lobe which come by way of 
the optic radiations and the posterior part of the internal capsule. 
These are the fibres of Gratiolet. 

The posterior quadrigeniiiial bodies receive fibres from the tem- 
poral lobe. The great development of these posterior bodies in whales 
leads to the supposition that they have something to do with the audi- 
tory nerve, by way of the nucleus acusticus. The maintenance of equi- 
librium, it must be remembered, is one of the functions probably of the 
semicircular canals. 

The anterior lobes of the quadrigeminal bodies picsent a micro- 
scopic appearance resembling layers of the cortical type, according to 
Spitzka. Outside are optic tract fibres, then a thin layer of small 
nerve-cells, then again some optic fibres and finally a layer of a few 
large cells. The posterior loins arc less striking in appearance and 



THE XOX-XEUROXIC DISEASES 



697 



merely contain some small cells and one nucleus filled with a network 
of fine fibres. The two posterior ganglia are connected by fibres that 
pass over the aqueduct of Sylvius. 

Beneath the corpora quadngemina are the peduncles of the brain, 
the aqueduct of Sylvius separating the corpora from the latter. I 
have already spoken of the substantia nigra lying in the middle and 
stretching transversely across each peduncle. The part above the 
substantia is the tegmentum; that below is the pes pedunculi. The 




glossopharyngeus 
N. vagoa. 



Nucleus n. cochlears dorsali 
[Nucleus tuberculi acustici] 



Tractus spinalis and nucleus tractus 
spinalis n. trigeiuini 

Nucleus n. vestibularis spinalis 
[Radix descendeo! ' 



Nucleus alac clnereae, tractus solitarius 
and nucleus tractus solitarii 
Ganglion cotnmissurale alaTe cinereat 



Diagrammatic representation of the nuclei of origin of the motor, and the 
primary terminal nuclei of the sensory cerebral nerves. (After Held.) 

substantia seems to be in part the termination posteriorly, in the 
stratum intermedium, of the fibre-system of the striate body. The 
real function of the gray matter we know nothing about. The tegmen- 
tum is the great sensory tract and contains the decussating fibres of the 
anterior cerebellar peduncle which connect upon Opposite sides the 
cerebellum and the red nucleus of the tegmentum. 

The pes pedunculi, below the substantia nigra, contains the great 
efferent system-fibres from the cortex. According to Dejerine, the 
fibres in the outer fifth of it arise from the middle part of the temi>oral 
lobe. The median fifth fibres come from the operculum. The middle 
three-fifths of the pes contain fibres from the posterior portion of the 






698 



THE XOX-XEUROXIC DISEASES 



frontal lobe and the central convolutions. This is the pyramidal tract, 
or tractus cortico-spinalis. 

Behind the quadrigeminal bodies, in the central gray matter, ap- 
pear the first of the cranial nerve nuclei — namely, the collection of 
cells along side of the aqueduct of Sylvius, that give rise to the oculo- 
motorius nerve. These nuclei deserve special consideration as local- 
ization symptoms in connection with them are often very definite. 

Cranial Nerve Nuclei. — These nuclei or ganglionic masses are in 
all respects the homologues of the anterior horns of the spinal cord. 



Anterior median (small- 
celltd) nucleus 



Edinger-WestphaV s nucleus 
[median and lateral groups) 



Central-median 
sagittal nucleus 

Lateral (large-celled) 
oculomotor nucleus 



Mixed trochlear oculo- 
motor nucleus 



Trochlear nucleus 



Trochlear nerve- 
Post, longitudinal fasciculus 




Trochlear decussation in the velum 

Grouping of the nuclei of the oculomotor region. Schematichorizont&l section. 
( Aiter Siemerliug.) 

They give origin to motor cranial nerves or to the motor strands of the 
cranial nerves and, like the spinal motor cells, preside over their nutri- 
tion. They are to be found along the aqueduct of Sylvius, in the floor 
of the fourth ventricle and in the deeper parts of the pons and medulla. 
It may appropriately be mentioned in this connection that the 
ganglia on the sensory cranial nerves are the homologues of the gan- 
glia on the posterior spinal nerve roots. In the development of the 
cephalic portion of the neural crest in the embryo there appear five 
pairs of ganglia, which gradually shift their position to the ventral side 
of the brain. They are the jugular, petrosal, geniculate, auditory and 
Gosserian ganglia. From them originate the sensory parts of the 
pneumogastric, the glosso-pharyngeal and facial nerves, all of the 



THE NON-NEURONIC DISEASES 699 

auditory, and sensory part of the trifacial. In all of these ganglia, 
except the auditory, the cells become unipolar. The single process di- 
vides T-like into peripheral and central fibres, just as they do in the 
posterior spinal ganglia. The central process assumes all the appear- 
ances of a neuraxone ; the peripheral that of a modified dendrite. The 
auditory ganglion moves backward to a point behind the geniculate 
ganglion. Its dendrites run outward to their termination in the 
acoustic apparatus of the ear. Its axones penetrate the medulla. The 
central axones of the other ganglia give of! numerous collaterals, enter 
the brain and divide T-like. They pass up and down and arborize 
chiefly in the terminal nuclei of the respective nerves, some of them, 
the excito-reflex fibres, terminating in the nuclei of the motor nerves. 

The similarity between the cranial nerves and the spinal nerves is 
thus made obvious and the contention upheld that the brain in a large 
measure, at least, is but a highly developed and much rearranged por- 
tion of the serial ganglia that constitute the entire cerebro-spinal axis. 

Xucleus of the Motor-Oculi Nerve. — This nucleus lies in the floor 
of the aqueduct of Sylvius. It consists of a number of subsidiary 
nuclei that supply the different muscles that rotate the eye ball, that 
contract the pupil and that elevate the lid. The nucleus is connected 
with those of the fourth and sixth cranial nerves behind it by means 
of fibres running in the posterior longitudinal bundle. It is also con- 
nected with the optic nerve, but just how is still a matter of dispute. 
Some authors state that the ocular facial nerve strands arise in the 
distal part of the nuclear area of the third nerve, though this is contra- 
dicted by Scruff, Cassirer, Siemerling and others. In the third or 
-oculomotor nucleus the subsidiary nuclei are arranged somewhat thus 
antero-posteriorly. 

Median Line. 
Sphincter iridis. Musculus ciliaris. 
Levator palpebral. Rectus interims. 
Rectus superior. Rectus inferior. 
( )bliquus inferior. 

The neuraxones from these little groups of cells enter the third 
cranial nerve and terminate in the correspondingly named muscles. 
The same may he said of the nuclei of the fourth and sixth cranial 
nerves lying still farther posteriori}- and sending their stimulation re- 
spectively to the superior oblique and external rectus muscles of the 
eye. Note that the sixth fibres do not decussate; all the others do. 

The posterior longitudinal fasciculus, that I said a moment ago 
connected the various subsidiary parts of the third nucleus, also in all 
probability connect all of the cranial nuclei. It extends much farther 
f< rward than the third nucleus. In all vertebrates it extends from the 
interbrain to the region of the anterior columns of the spinal cord, and 
is thus one of the fundamental features of the brain. In a way it be- 
longs to the pyramidal system. 

Trigeminal Xucleus. — The sensory fibres of the fifth cranial nerve 
arise, as I have stated, from the < rasserian ganglion resting on the 
petrous part of the temporal bone. The central ends of these neuron,- 



700 



THE N0N-NEUR0NIC DISEASES 






ramify in the sensory nucleus of the preoblongata. They divide, just 
like the central ends of the spinal sensory neurones do in the columns 
of Burdach, into a descending branch, which forms the spinal or long- 
root of the trigeminus, and an ascending branch. The collaterals from 
these up-and-down branches arborize and ramify in the neighboring 
gray matter, which is continuous with the spinal substantia gelatinosa 
and surround the cells therein found. It is believed that collaterals also 
extend to the facial and other cranial nerve nuclei. The pontile por- 
tion of the nucleus, according to Kolliker, is only the beginning of the 
gray matter. It is thus made plain how the components of the fifth 
nerve represent the sensory correspondents of the third, fourth, sixth, 

FIGURE 174. 



™" IV 





— Sections through the origin of the focrth nerve (Stilling). £ 

A, transverse section at the place, of emergence of the nerve-fibres. B, oblique section 
carried along the course of the bundles from the nucleus of origin to the place of emer- 
gence. Aq, Sylvian aqueduct, with its surrounding grey matter ; IV, the nerve-bundles 
emerging ; IV\ decussation of the nerves of the two sides ; IV", a round bundle passing 
downwards by the side of the aqueduct to emerge a little lower down ; ?i, IV, nucleus of 
the fourth nerve. /, fillet; s. c. p., superior cerebellar peduncle; d.V., descending 
root of the fifth nerve ; pi, posterior longitudinal bundle ; r, raphe. 



motor branch of the fifth, the seventh and the twelfth nerves. Instead 
of remaining separated as they are in the cord below, the sensory 
paths have here all become amalgamated into the fifth nerve, while the 
motor correspondents still remain separated. 

It is believed from recent investigation that the proximal part of 
the trigeminal root fibres correspond to the third branch of the nerve, 
while the distal part corresponds to the first. 

The motor root springs, of course, from the large-cell motor nu- 
cleus. There is also a cerebral root to this nerve, called the mesen- 
cephalic, because it has its origin in the pregeminal region just in front 
of the aqueduct of Sylvius. This is probably a motor root. 

Facial Nucleus. — This is a large-cell nucleus, homologous to the 
anterior horn of the cord, and lies mesially to the spinal trigeminal in 
the lower part of the pons. After joining, the processes from its cells 
curve in a bundle around the sixth nucleus and then continue obliquely 
outward and downward between the facial nucleus and the trigeminal 
root. The two facial nuclei are connected by commissural fibres. 

The nerve of Wrisberg has its origin apparently from the ganglion 



THE X0X-XEUR0X1C DISEASES 



701 



^eniculi and is thus a part of the sensory glossopharyngeal root. By 
this nerve the chorda tympani becomes united with the glosso-pharyn- 
_geal nerve or the solitary fasciculus. Thus is explained the visceral 
function of the facial nerve as seen in the taste phenomena related to 
the chorda tympani. 

The facial nucleus belongs to the series of the motor nuclei of 
the ninth, tenth and eleventh nerves, which represent the upward 
prolongation of the lateral and anterior gray matter of the cord. The 

FIGURE 176. 




a0& 



Fare? 



Cross-section through the medulla at the height of the entrance of the acoustic ( Enlargement 
.1.) VHP, ventral acoustic nucleus; VIII*, dorsal acoustic nucleus; N. C, cochlear nerve ; 
Pc, cerebellar peduncle (restiform body) ; R.d. VIII, descending acoustic root ; Slr.ac. , acoustic stria ; 
co, cerebello-olivary fibres, etc. (After Kolliker.) 

nucleus receives a cortical stimulus by way of the fibres that course- 
down through the anterior part of the posterior limb or knee of the 
internal capsule. These fibres lie in the crusta to the inner side of the 
pyramidal tract. They decussate before reaching the nucleus. 






702 



THE N0N-NEUR0NIC DISEASES 




THE XOX-XEUROXIC DISEASES 



703 



Auditory Nuclei. — Innervating the cochlea and semicircular canals 
of the internal ear, the auditory nerve contains fibres that subserve 
different functions — namely, hearing and space-sense appreciation, and 
hence has two sets of nuclei. The nerve enters the medulla by the 
two roots, lateral or posterior and median or anterior. These roots 
are connected with three nuclei. The cochlear root processes terminate 
and arborize in the accessorius, or ventral acoustic nucleus and acoustic 
tubercle that lie in the substance of the lateral root and between it and 

FIGURE 177. 




Nucleus n. vesti- 
bularis superior _ 
(Fleebsig, Bechterew) 
Nucleus n. vestibular! 

inediMU [Schwalbe 



Format io reticularis- 



Corpus restiformc 

Radix n. vestibularis 
and nucleus n. vesti- 
bularis lateralis 
|Deitcrs| 



Radix n coctalearis 



Traclus spinali>_-. ~]^H 
d. irigeuiiDi 1 - - ' 








n. facialis j . J 






inKrolivarc^-^^^^A ■■ Hk ^Kk 
lemnisci - ~^^^^B lA^fl ^JjfX. 


affi y 


>■!<= 






f V 


r\f 


Radix 
vestibularis 


.Nucleus arcuntus 


Nucleus oUfMla tnfc 


Pons [Varuli] 
rior 




Pyrarnis [nicdul'ac qbl<>". 









Section through the middle of the cerebellum and through the medulla 
oblongata. (After Flechsig and Held.) 



the median root. They are the pathway of the auditory impressions and 
arise in the spiral ganglion of the cochlea. They probably connect 
somewhat also with the other ganglia or nuclei. The vestibular root 
processes originate in the ganglion searpae <>f the labyrinth and instead 
of hearing, have the function of sending coordinating impulses to the 
central organ, particularly the cerebellum. Their central arborizations 
are in the dorsal central inner nucleus or chief nucleus and the large 
cell nucleus of Dieter and the continuation of this in the vestibular 



704 



THE N0N-NEUR0NIC DISEASES 






nucleus of Bechterew. This vestibular pathway is not only continued 
up into the cerebellum, but it seems to run down towards the spine in 
a tract which is a continuation of the funiculus cuneatus (Burdach's 
column). It is known as the descending acoustic root. The acoustic 
strict seen running across the floor of the fourth ventricle is a sensory 
tract from the acoustic tubercle that decussates in the raphe and con- 
tinues on into the lateral lemniscus. 

The accessory nucleus sends its cell processes up through the 
lateral lemniscus to the posterior corpora quadrigemina and so on to 

FIGURE 178. 




Posterior view of the medulla oblongata, the fourth ventricle and the severed 
cerebellum. 1, fourth ventricle; 2, striae acusticse; 3, posterior cerebellar pedun- 
cle; 4, fasciculus gracilis; 5, anterior cerebellar peduncle; 6, fillet; 7, middle cere- 
bellar peduncle; 8, corpora quadrigemina. (Affer Hirschfeld and Leveille.) 

the first and second temporal convolutions. Some fibres pass directly 
through the lemniscus and tegmentum to the temporal lobe without 
going to the posterior corpora quadrigemina. This nucleus connects 
also with the superior olivary bodies, with other cranial nuclei, and by 
way of the acoustic stria? with the formatio reticularis, sensory tract, 
posterior corpora quadrigemina and temporal cortical area. 

The Dieter's and chief nuclei send their processes to the direct 
sensory cerebellar tract and thence to the red nucleus of the tegmentum 
and the emboliform and globose nuclei of the cerebellum. 

Vago-glosso-pharyngeal Nucleus. — The nuclei of the ninth and 
tenth cranial nerves cannot well be separated. The sensory branches 
have the cell bodies of their neurones nesting in their respective 
ganglia on the roots. From thence the central processes enter the 
brain, divide T-like and send one branch downward and the other 
upward. The downward brandies constitute what used to be called the 
ascending root of these nerves. They give off collaterals. This so- 
called ascending root is the solitary bundle or fasciculus. It receives 
the central terminations of the neurones in the root ganglia (jugular, 



THE XOX-XEUROXIC DISEASES 



7"5 



petrosal, plexiform, etc.) of the vagus and glosso-pharyngeal nerves. 
It sends its own processes on up into the brain. The motor branches 
of these nerves arise from one common nucleus, the nucleus ambigaus. 

The accessory branch of the eleventh or spinal accessory nerve 
arises from the nucleus ambiguus. The nucleus is probably homo- 
logous in some respects to* the column of Clarke. The motor branch 
of the spinal accessory nerve arises from a group of cells in the an- 
terior horns of the cervical coid reaching from the first nearly to the 
sixth cervical segment. Its representation in the upper three segments, 
however, is the most important. 

Hypoglossal Nucleus. — This nucleus is the homologue of the an 



FIGURE 179 




II. 



e 


a|^H|=^ 









Section of cerebellar cortex, stained by Golgi's method ; 1 . taken across the 
lamina; n. in the direction of the lamina; a, outer or molecular layer; b, inner or 
granular layer ; c, white matter, o, Cell of Purkinje ; b, small cells of inner layer ; c, 
dendrons-of these cells ; d, axis-cylinder process of one of \heae cells becoming longitu- 
dinal in the outer layer ; e, bifurcation of one of these ; g, a similar cell lying in the 
-white matter. (Ramon y Cajal.) 



terior horns of the cord and of the nuclei of the third, fourth and sixth 
nerves. It lies near the raphe in the lower part of the floor of the 
fourth ventricle. Jts cells are large and it has a rich network. hi 
some lower animals the hypoglossal is a pure spinal nerve. 

There are some minor nodal nuclei and other small deposits of 
gray matter in addition to these to be found in the after-brain or 
medulla. 

The Olivary Bodies are two large ganglia lying on either side of 
the after-brain. They connect with the cerebellum, hnt of their func- 
tions we know nothing. 

Cerebellum. — The cerebellum lies beneath the posterior part of 
the cerebrum; consists of a middle and two lateral lobes; and is con- 
nected with the cerebrum above and tin- COrd below. The two sides 

the cerebellum are united by pontile fibres. In general structure it i^ 

not very unlike the cerebrum. The vermis, or middle lobe, and the 



706 



THE NON-NEURONIC DISEASES 



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THE NON-NEURONIC DISEASES 



707 



hemispheres are divided into lobe? and lobules and fantastically named. 
The gray matter or cortical layer on its surface is so minutely and 
peculiarly folded that with its intervening white matter it gives the 
appearance of an arbor vitas. In the center of the white substance is 
the convoluted nucleus called the corpus dentatum, or ciliary body. 
Other nuclei are the cnibolifonn, fastigium and globosus. 

Cerebellar Cortex. — This is a remarkable arrangement of neu- 
rones. With the lew power of magnification it can be seen that there 
are three distinct layers; externally the zona molecularis, internally 
the zona granulosa, and between the two the layer of the large cells 

FIGURE 181. 



Nucleus 
lcntlformi! 



Capsula externa 

Capsula interim 




N. cochlear)! 
Nucleus n. cochlearis ventralis 

Tnbcrculum acuslicinu 



Illustration to show the course of some of the more prominenl conduction 
paths in the brain. (After Held.) 

of Purkinje. These cells of Purkinje arc among the largest in the 
nervous system, measuring from 1-800 to [-600 1 1" an inch. They pos- 

also large round nuclei. Each cell sends a neuraxone down into 
the zona granulosa, on the way giving off collaterals that bend around, 
pass upward and break up into branches, around the cell-body. The 
dendritic processes arc enormously profuse and extend up toward and 
almost to the edge of the cerebellum. The profuseness of the dendritic 
elaboration is best seen in a section made in the sagittal plane. 

Among the profuse dendritic branches are mingle. I thick fibres oi 









708 



THE NON-NEURONIC DISEASES 



unknown origin, though they apparently have come in from the white 
substance crossing the zona granulosa. Among them are other, small. 
stellate cells, which send their processes here and there parallel to the 
surface of the cortex and down to the bodies of the Purkinje cells, 
which they surround with their terminal arborizations in such a basket- 
like way that they have been called basket-cells. These smaller cells 
that obviously have given the name molecular layer to this outermost 

FIGURE 182. 







Illustration to show the course of the pyramidal tract and of the cerebro- 
pontile paths; the termination of the auditory conduction path and the indirect 
continuation of the medial lemniscus and the brachium conjunctivum from the 
lateral nucleus of the thalamus. (After Held.) 

part of the cortex serve well as inter-communicating elements between 
the individual Purkinje cells. 

The granular layer is made up chiefly of small polygonal cells with 
large nuclei, measuring about 1-5000 inch in diameter. They have 
short dendrites with clubbed extremities and a neuraxone. The latter 
passes up to the molecular layer, where it divides into two branches 
which run transversely to the axis of the body of the cell. There are 
in the granular layer also cells of the Golgi type, large, with axis 



THE XOX-XEUROXIC DISEASES 



709 



cylinders that divide and subdivide and end in a finely ramifying 
plexus. 

The fibre systems of the cerebellum, like those of the cerebrum, 
are tangential and radiating. The complicated arrangement of the ele- 
ments of the cerebellar cortex and their character suggest the possi- 
bilitv of an enormous number of combinations. Hence it reveals a 



FIGURE 183. 




Illustration to show the position of the pyramidal tract, the secondary optic 
radiation, the fronto-pontile path, the temporo-pontile path, the auditory con- 
duction path, the primary optic radiation, the medial lemniscus, the hrachium 
COnjunctivum, the lateral areas of the formalin reticularis, and the cortical path 
from the lateral nucleus of the thalamus. (After Meld.) 

marvelous condition fur bringing together and coordinating and har- 
monizing the activities of a greal many diverse elements. The large 

cells being so comparatively less numerous than the small, W e 
that the cerebellum is a great receiving or way station for impulses 

traveling between the brain and the periphery. It adjusts nerve im- 
pulses and coordinates their further distribution. 



yiO THE NON-NEURONIC DISEASES 

The Conducting Tracts of the Brain. — In the brain, as in the cord, 
the same laws in regard to the degeneration of the neurones when 
separated from their nutritive centers in the cells hold true. By this 
means the tracts of the brain and the tracts between the brain and 
cord have been largely traced. In our stud}- of the minute anatomy 
of the brain most all of these tracts have been mentioned. It may be 
well to briefly recapitulate them here. The reader is also referred to 
the chapters on the neuronic architecture and on the anatomy and 
physiology of the cord. 

The calculation has been made that only about one-third of the 
brain cortex is involved in the projection tracts. The remaining two- 
thirds do not send processes out to or receive processes directly from 
the periphery. This two-thirds is intimately inter-connected by asso- 
ciation, commissural and other intercalated tracts. 

The motor projection tracts start from the cells of the central con- 
volutions of the cortex and pass down through the internal capsule to 
the various cranial nuclei and anterior cornua of the spinal cord, as 
has been previously explained. It is throughout a crossed tract, though 
the crossing does not occur at the same place for all parts of it. The 
parts that pass to the cranial nuclei we cannot trace as clearly as 
some other parts, but we believe they decussate just before they reach 
the respective nuclei. Of the remainder of the tract, nine-tenths of it 
decussates in the pyramidal decussation of the medulla, and one-tenth 
crosses over lower down in the anterior commissure of the cord. 

The sensory projection tracts are more complicated and less well 
known than the motor. Those of the posterior columns of the cord 
terminate in the nuclei of the medulla found at the top of these 
columns. Thence the tract continues across to the other side in the 
lemniscus or fillet decussation (internal arciform fibres, midolivary 
strata, chief lemniscus), and so on up to the cortex directly or after 
interruption in the optic thalamus, or possibly also in the lenticular nu- 
cleus. Another sensory pathway is the antero-lateral, Gowers' column, 
the chief lemniscus of the medulla and cortex directly or after interrup- 
tion. It terminates in the central convolutions, parietal areas and gyrus 
fornicatus. 

The tracts from the sensory cranial nerve nuclei, the nucleo-cor- 
tical tracts, are very little known. They decussate in the raphe or 
perhaps pass through the chief lemniscus. 

Many are the ways in which sensory impulses reach the brain, and 
for aught we know, there may be more intermediary neurones than 
have so far been described in each tract. 

The cerebellar tracts, the visual tracts and others have all been 
sufficiently noted when describing the cerebellum, optic nerves, ete. 

CIRCULATION OF THE BRAIN. 

Before passing on to the consideration of the physiology of the 

brain, some note must be taken of its circulation. Including the scalp, 
the skull and the dura mater, the head and its contents are furnished 
with blood by way of the external and internal carotids and the verte- 
bral arteries, the latter f: rming the basilar artery. 



THE NON-NEURONIC DISEASES 711 

The external carotid supplies the outside of the head, sending into 
the interior of the cranium only meningeal arteries. These meningeal 
branches include the inferior meningeal, the posterior meningeal, the 
middle and small meningeals. 

Of all the meningeal arteries the middle meningeal is the most 
important, because it is the largest, is most direct in its communication 
between the outside and inside of the skull, and its area of distribution 
is related to parts of the brain of great functional significance. The 
blood returning from the meninges empties into the diploic veins and 
thence passes to the lower occipital and lateral sinuses. The venae 
comites carry some of it. 

The internal carotid has no branches in the neck. It supplies the 
interior of the cranium by means of its anterior meningeal branches, 
anterior and middle cerebral, posterior communicating and anterior 
choroid branches. 

The basilar artery terminates in the posterior cerebral, anterior, 
superior and inferior cerebellar and posterior meningeal branches. 

The inter-communication of the branches of the internal carotid 
in front and the basilar behind forms at the base of the brain a remark- 
able anastomosis known as the circle of Willis. This circle of Willis 
is really a heptagon and reaches from a point in the longitudinal fissure 
in front of the optic chiasm back to the edge of the pons Varolii. It 
measures about an inch in width and is an inch and a half antero-pos- 
teriorly. Its front limitation is formed of the anterior cerebral arteries 
that have just left the internal carotids and that are united by the 
transverse anterior communicating artery. Its lateral boundaries are 
made up of the posterior communicating arteries which form an anas- 
tomosis between the internal carotids and the posterior cerebral arteries 
which bound the circle behind. This circle of Willis supplies especially 
the midbrain and the basal structures. The midbrain receives blood 
also from the superior cerebellar arteries. 

The cerebral cortex and white substance, together with the pia 
mater, receive their vascular supply from the large distal branches of 
the cerebral arteries. The internal ganglia and interbrain are fur- 
nished by the small proximal branches. It is both convenient and 
physiological, therefore, to discuss the blood supply of the cerebrum 
under the heads of the cortical system and the ganglionic system. The 
choroid system should also be taken into special account. 

Cortical System. — Entering the front lower part of the longitudinal 
fissure, after winding around the genu of the corpus callosum, the 
anterior cerebral arteries pass backward along the mesial surface of the 
hemispheres as far as the parietooccipital fissure. From each artery 
Spring the anterior internal frontal, supplying the internal orbital eon 
volution, olfactory bulb, superior frontal and anterior half of the mid- 
dle frontal convolutions; the middle internal frontal supplying the 
Corpus callosum, the gyrus fornicatUS, marginal gyrus and upper end 
of the ascending frontal convolution : and the posterior internal frontal, 
supplying the quadrate lobule and part of Hie superior parietal convo- 
lution. 

In the Sylvian fissure runs a most important artery, the middle 



712 



THE XOX-XEUROXIC DISEASES 



cerebral. This has four branches. Of these the external and inferior 
frontal furnish blood to the anterior and posterior orbital and third 
frontal convolutions ; the ascending frontal and ascending parietal 
carry it to the convolutions of the same name ; and the parietotemporal 
supplies it to the supra-marginal, angular, superior and middle temporal 

FIGURE 184. 




The arteries at the base of the brain. (After Monakow.) Acera, anterior cerebral artery 
Coma, anterior communicating artery ; A FSy, artery of the Sylvian fissure ; Alcnt, lenticular artery 
1-5, the cortical chief branches of the Sylvian artery ; cp, posterior communicating artery Acha 
anterior choroid artery ; x, lateral branches of the posterior communicating artery'; Acp, posterior 
cerebral artery ; Abas, basilar artery ; At, temporal artery ; Aocc, occipital artery , A ccrsup, suwricr 
cerebellar artery ; A cer med, median cerebellar artery ; A cer ivf, inferior cerebellar artery 
anterior spinal artery. 



Three cortical branches spring from the posterior cerebral arteries 
and cover the tentorial area of the brain. The occipital goes to the 
aniens and cortex of the occipital lobe ; the uncinate supplies the un- 
cinate convolution (the hippocampal and lingual areas)"; and the tem- 
poro-sphenoidal carries its blood to the fourth, third and part of the 
second temporal gyri. 



THE XOX-XEUROXIC DISEASES 



7*3 



Ganglionic System. — This system is constituted of the small ar- 
teries of the circle of Willis and cerebral arteries. Generally six groups 
of vessels are recognized. Some of these are of immense importance 
to the pathologist and clinician. 

The antero-incdian ganglionic arteries originate in the anterior 
cerebrals and the anterior communicating. They penetrate the lamina 
cinerea and a few of them supply the head of the caudate nucleus and 
anterior wall of the third ventricle. 

FIGURE 185. 

re 




Lateral view of the right hemisphere showiDg the area supplied by the middle cerebral artery. 
(After Monakow.) Art.F.S., artery of the Sylvian fossa; I-V, the five chief branches of this 
artery; Ft, central fissure; FS, Sylvian fossa; OP., interparietal fissure; I, first temporal fissure; 
Fi-F 3 , first, second, and third frontal convolutions ; SM, supramarginal gyrus ; Ang, angular gyrus ; 
0i-03. first, second, and third occipital convolutions. The dotted line shows the area supplied by 
the Sylvian artery. 



The antero-lateral ganglionic arteries, making up the second and 
third groups, arise from the middle cerebrals just outside of the circle 
of Willis. They penetrate the anterior perforated space and carry 
blood to the corpora striata, internal capsules and optic thalami. 'Hie 
lenticulo-striate artery of this group, tint supplies the entire striate 
body, is sometimes called, On account of the frequencj <>!' its rupture, 
the artery of cerebral hemorrhage. 

The postero-median ganglionic arteries are branches of the ■ 
terior cerebral and posterior communicating arteries. The inter- 
peduncular structures and crustae receive their blood fr-nn them and 
after piercing the posterior perforated lamina they supply the walls 
the third ventricle and the mesial parts of the optic thalami. 






714 THE NON-NEURONIC DISEASES 

The fifth and sixth groups are made up of the poster o-lateral 
ganglionic arteries. They spring from the posterior cerebral arteries 
after the latter have wound around the crura and are distributed to the 
posterior parts of the optic thalami, the corpora quadrigemina and the 
corpora geniculata. 

These ganglionic arteries do not anastomose with one another or 
with other cortical arteries . They belong to the Cohnheim type of 
terminal arteries. On account of the relatively poor blood supply of 
the brain between the cortical and ganglionic systems, this area is par- 
ticularly liable to encephalomalacia. 

The choroid arteries are three in number. The anterior choroids 
spring from the internal carotids, enter the apices of the descending 
horn of the lateral ventricles and supply the inferior two-thirds of 
the choroid plexus, part of the velum interpositum, the hippocampus 
major and corpus fimbriatum. The posiero-lateral choroids originate 
in the posterior cerebrals and are distributed to the upper third of the 
choroid plexus of the lateral ventricles and to the velum interpositum. 
The postero-medial choroids also start from the cerebral arteries and 
supply the choroid plexuses of the third ventricle and its velum inter- 
positum. The velum interpositum also receives branches from the 
superior cerebellar arteries. 

Veins. — The vena cerebri magna, common vein of Galen, collects 
the blood from the velum interpositum, the lateral and the third ven- 
tricles. The superior cerebral, medial cerebral and inferior cerebral 
veins drain the surface of the brain and empty into the neighboring 
sinuses. It may be of some clinical importance to note that the in- 
ferior cerebral veins, on the tentorial surface of the brain, empty into 
the petrosal sinuses against the current. 

Lymphatics are not found in the brain or cord, but there are 
perivascular lymph spaces. 

The pons Varolii, medulla oblongata and cerebellum are supplied 
by terminal branches wholly from the vertebral and basilar arteries. 
They are called nuclear and radicular arteries and need no special de- 
scription. The hypoglossal nerve root is furnished with blood by the 
anterior spinal artery ; the other cranial nerve roots get their supply 
from branches of the vertebrals. The olives and pyramids are supplied 
from either the vertebrals or the anterior spinals. The rest i form 
bodies get their supply from the inferior cerebellars, which also send 
branches to the roots of the vagus, accessorius, spinal root of the 
trigeminus and the reticular field generally. 

PHYSIOLOGY OF Till-; BRAIN AND CEREURAL LOCALIZ \- 

TION. 

The credit for the earliest suggestion that the brain is a composite 
rather than a single organ is usually given to the phrenologist. Gall 
( 1 758-1828), whose work Sur les Fonctions du Cervcau et sur Celles 
dc Chacune de ses Parties appeared in 1825. M. Farabeuf, the dis- 
tinguished anatomist of Paris, has discovered, however, a work by 
Joseph Baader, a professor at Freiburg-in>Bresgau from 1740 to 1750. 



THE NON-NEURONIC DISEASES 715 

in which it is clearly intimated that the sensory and motor functions of 
the brain may possibly be separated and localized. The work is entitled 
Observationes Mediccc Incisionibus Cadaverwm Anatomicis Illustra- 
tes, was published separately in 1762, and was reprinted in Sandifort's 
Thesaurus Dissertationuin in 1778. Notwithstanding these early hints 
at cerebral localization, the scientific world continued to believe with 
Flourens (1794-1867) that all the faculties occupied the same place, 
that to perceive and to will constituted essentially the same faculty, and 
that this faculty resided in a single organ. 

The mapping out of the brain surface into sensory, motor and other 
areas is distinctly a recent advance in physiology ; the explanation of 
the correlation of these areas, and of the dependence of mind upon 
brain, is still an unsolved problem. 

The subject of cerebral localization is one of unequal magnitude, 
according as it is looked at from the standpoint of the surgeon, the 
physiologist, or the psychologist. In its consideration the practical 
bearings have been so generally uppermost it has happened that only 
those parts of the brain have received the largest amount of study 
which could be reached by the surgeon's knife. Certain superficial 
sensory and motor areas have been the most completely established, 
though these areas probably represent the coarsest and most primitive 
functions of w T hich the brain is capable. It is obvious that other and 
deeper parts of the encephalon play an important, if not really a more 
important role in the tout ensemble of brain activity, and that the local- 
ization of the functions of these parts is quite as much of a desideratum 
scientifically as is the localization of the sensory and motor areas of 
the cortex. The physiologist is called upon to explain the function and 
presence of the following deposits of gray matter in the cranium, the 
localization phenomena of some of which are already fairly well 
understood : 

Cerebral cortex; olfactory lobes; corpora striata (caudate and 
lenticular nuclei) ; optic thalami (and pulvinar) ; corpora geniculate 
(external and internal); corpora mamillaria ; corpora subthalamica ; 
corpora quadrigemina (anterior and posterior) ; epiphysis; hypophysis; 
red nuclei ; substantia nigra ; cerebellar cortex ; cerebellar nuclei ; 
pontile nuclei; corpora olivaria ; nodal nuclei; cranial nuclei. 

These gray deposits have each their special raison d'etre, and all 
doubtless play their part in the sum total of brain activity. It is a 
matter of extreme difficult) and of inten.se interest to define accurately 
their functions. The more exact diagnosis of focal lesions and the 
more rational explanation of nientalization both call loudly for a solu- 
tion of this problem. The question involves more than that of making 
a mere surgical diagnosis; it involves tin- whole subject of normal an 1 
abnormal mental and cerebral phenomena. Physiology must here pro- 
ceed hand in hand with psycholog) and endeavor to localize the 
encephalic seat of such manifestations as memory, volition, intellection, 
imagination, etc., or at least the seat of their highest manifestation. 

For the practical purposes of diagnosis and surgical interference-, 
the study of the cerebral localizations must include also certain other 
parts of the encephalic m-'ss, a-, fi r instance, the centrum semiovale, 



yi6 THE NON-NEURONIC DISEASES 

the corpus callosum, the internal capsule, the crura cerebri and other 
association and projection tracts. 

In discussing, therefore, the cerebral localizations from the widest 
standpoint, one is obliged to discuss the function, or functions, of the 
entire encephalon, its psychoses as well as its neuroses. Only by such 
a wide discussion can one hope to avoid confusion and prevent the 
splitting up of the theme into disconnected and irrelevant facts. As our 
knowledge of the functions of each part of the encephalic mass becomes 
more precise, the so-called schools of loealizationists become more and 
more amalgamated. 

Among the investigators of cerebral localization there are at pres- 
ent three schools of varying degrees of prominence. In a general 
way, it may be said that the English-speaking physiologists regard the 
sensory and motor areas of the brain as more or less separate and dis- 
tinct, and as centers for the direct reception and emission of sensory 
and motor impulses. The Germans incline to the view that these areas 
are the centers for the direct reception and emission of nervous im- 
pulses, but that they coincide or more or less intermingle. The French 
and Italian investigators study the question more from the psycho- 
logical side, and place less stress upon the separation or commingling 
of the sensory-motor areas than they do upon the doctrine that the 
cortex is a general center for the representation of motor and sensory 
images. Psychosis, according to the latter, is a sensory-motor phe- 
nomenon, and mentalization is the product of the combined activities 
of the sensory and motor areas. They hold that the direct sensory- 
motor elements are lower down than the cortex ; that impulses of 
cerebral origin are as much peripheral as are those starting from the 
skin ; and that voluntary action is as much of a reflex as is an ordinary 
involuntary spinal reflex. This of course is a mere outline statement 
of the three views in vogue. 

Before taking up cerebral localization in detail, I desire to empha- 
size the fact that many of the higher so-called cortical centers subserve 
in some prominent, yet unaccountable, way very complicated psycho- 
physical processes. Such processes, for instance, are speech, writing, 
reading. And yet these are doubtless very elementary psycho-physical 
processes in comparison with those that probably underlie what are 
called imagination, reasoning and general intellection. 

It has always seemed to me to be a crude conception of psycho- 
logical processes of all sorts to suppose that they were each individually 
under the absolute and sole control of certain small areas in the cortex. 
The sharp differentiation made by some physiologists between the 
cortical centers, the narrow way in which they limit them and the dis- 
tinct functions which they assign to them, as though there were hardly 
any commingling or interconnection between them, has long seemed to 
me to be puerile, grossly materialistic and absolutely unwarranted by 
any scientific proof worthy of the name. 

There is no doubt that the brain, like the spinal cord, is a great 
compound and complex organ. It has relatively independent functions 
in its various parts. These parts and functions, however, are never 
absolutely independent. Their independence is only so far as they 



THE NON-NEURONIC DISEASE- 717 

subserve the particular purposes of motion and sensation. So far as 
we now know, there is only one type of motor impulse, five of sensory 
impulses which again are somewhat subdivided. The former are 
emissive, the latter are receptive. Beyond these we know of no dis- 
tinct, well-defined impulses passing- in or out of the brain. 

I have referred to all of this elsewhere. I repeat it here because 
I desire to emphasize the distinction between these ingoing and outgoing 
impulses, and what is called psychosis. A psychosis is distinctly not 
the same as a motor or a sensory impulse. A psychosis is a compound, 
complicated phenomenon. Its elements are motor and. sensory, but it 
itself is a combination of elements. A psychosis is, therefore, most 
emphatically a function. The function is the interplay and inter- 
mingling of the elementary motor and sensory elements in such a wax- 
as to eventuate in the psychosis. If the basic elements are normal and 
the interplay is normal, or according to commonly accepted standards, 
the psychosis will be normal. If the basic elements, wholly or in part, 
are disordered, or if their inter-connections and inter-relationships are 
abnormal or different from the commonly accepted standards (as de- 
picted in the relative degrees of intelligence, education, etc.), the psy- 
chosis will actually be, or seem to be, abnormal. This is a psychological 
truth boldly and briefly stated here because space will not permit of 
further elaboration of it. 

The reader who wishes to study this view of the mind for himself 
is referred to the writings of Wundt, the leading exponent of modern 
physiological psychology. 

Speech, reading and writing, as I have pointed out elsewhere, arc 
not mere motor and sensory phenomena. They are the expression of a 
high order of psychosis. It follows, therefore, that they are not sub- 
served alone by fixed small centers in the cortex, but by most compli- 
cated intra-cerebral mechanisms, of which the so-called cortical centers 
are but the prominent outposts, as it were. 

All statements, therefore, such as that the anterior lobes subserve 
the higher mental powers; that Broca's center regulates motor speech; 
that the occipital lobe is the memory center for visual images, must 
be taken only relatively. In every complicated act that is more than a 
mere emission of a motor impulse, or the reception of a simple sensory 
impulse, in a word, in every psychic phenomenon, however small or 
vast it may be, so long as it is psychic and indicates psychic process 
the whole brain must be conceived as taking a greater or less part in 
the process. Psychosis is a brain function, not a function of its mere 
constituents. 

With this understanding of the nature of what are called the 
cerebral localization centers, 1 will proceed to discuss them briefly in 
detail. 

The Cerebral Cortex. — Local disease of the prefrontal lobes docs 
not give rise to any very definite localizing symptoms. It has been 
determined experimentally that at the base of the first and second 
frontal convolutions is a small area which controls tin- lateral move- 
ments of the head, tin- elevation of tin- eyelids, and the dilatation of the 
pupils. This has not been well established in man, however. Aside 






7 i8 



THE NON-NEURONIC DISEASES 



from these areas, the prefrontal lobes are usually credited with the ex- 
pression of the higher intellectual life. It has been observed that lesions 
of these lobes cause a change in the disposition and temperament, a 
lack of self-control, undue irritability, loss of the power of attention, 
loss of memory, general apathy, foolishness, and a tendency to laugh 
and cry immoderately without adequate cause. According to Flechsig, 
a delirium of grandeur accompanies irritative lesions, to be followed 
later on by a loss of judgment and general mental hebetude. 

Phelps has recently analyzed 295 cases of brain injury and con- 
cludes that the frontal lobes, and especially the left frontal lobe, is the 



FIGURE 186. 




Schematic representation of the left cerebral hemisphere, showing the known 
cortical centers in man. 

seat of the higher mentalization phenomena. It has been long recog- 
nized that the entire left side of the brain is superior to the right, but 
it is startling to learn that we only think with our left frontal lobes. 
Phelps observes that in every instance in which a laceration was con- 
fined to the right lobe, the mental faculties were unaffected. This may 
explain some of the puzzling cases in which brain injury sometimes 
profoundly affects the mind and sometimes does not. 

In calculating the degree of mental deterioration, the observer 
must give due consideration to the patient's previous mental capacity. 
No motor or sensory symptoms are awakened by lesions limited to the 
prefrontal lobes. If the lesion, such as, for instance, a tumor, increases 
in size so as to produce an irritative, followed by a destructive, change 
in the neighboring convolutions, the above-mentioned symptoms will 
be accompanied by "neighborhood symptoms." Anosmia has been 
observed to follow disease of the basal parts of these lobes, but it may 
he. a mere "neighborhood symptom" due to their proximity to the 
olfactorv lobes and tracts. 



THE NON-NEURONIC DISEASES 7IO, 

According to Brims, Oppenheim, Bernhardt and others, tumors 
of the frontal lobes cause a disturbance of equilibrium identical with the 
so-called cerebellar ataxia. Moeli and Wernicke had already made 
mention of this frontal ataxia. A tract from the frontal lobe descends 
in the median part of the foot of the cerebral cms as far as the nuclei 
of the pons. These nuclei are connected by fibres running through the 
middle peduncles with the cerebellar hemisphere of the opposite side. 
Bruns, who was the first to call special attention to the probable cause 
of this frontal ataxia, argues that the highest volitional centers for 
the great trunk musculature send impulses to the cerebellum by way 
of this fronto-ponto-cerebellar tract and thus exercise a certain voli- 
tional control over the latter's coordinating function. Much uncer- 
tainty surrounds our knowledge of this tract, however. Mills declares 
that, in his experience, pure, uncomplicated disturbance of equilibrium 
resembling cerebellar ataxia has not often been present in tumors of 
the frontal lobes. In two cases of cerebral tumor reported by Wiener, 
in which the neoplasm encroached upon the frontal lobe, there was 
prcnounced ataxia. It may be that in certain cases of internal hydro- 
cephalus in which there are a peculiar staggering gait resembling that 
of cerebellar ataxia and an absence of indications of pressure in and 
around the fourth ventricle, as in a case recently brought to my clinic, 
the ataxia is due to pressure upon the frontal lobes by the fluid in the 
lateral ventricles. Ataxia, when a symptom of cerebral disease, ap- 
pears under three forms, each being caused respectively by lesions in 
the motor region, in the internal capsule, and in the parietal lobe. 

The sensorial areas of the cortex are made at the present day to 
include the gyrus fornicatus (Ferrier, Schafer, Horsley and Flechsig), 
the hippocampal convolution, the precuneus, portions of the parietal 
convolutions (von Monakow), and the posterior part of the central 
convolutions (Flechsig, Hosel). In a general way the sensory area 
includes the postero-parietal parts of the hemispheres. This seems to 
be well established b\ pathological observations in man, as well as by 
experimentation upon animals. It must be remembered that Ferrier's 
observations in regard to the centers of sensation were made mostly 
upon monkeys and the lower animals and that focal epilepsies, which 
finally terminate in a general convulsion, indicate that the human is far 
higher and more intricate in structure than is the animal brain. 

It is greatly to be regretted that patients presenting symptoms of 
a lesion in the motor zone of the cortex are not more frequently and 
minutely examined with regard to general sensation. In many of the 
cases of paralysis reported in literature there is no mention whatever 
sensation; and in others in which the attempt has been made to 
discover the sensibility of the skin, the methods adopted haw been so 
crude and unscientific, and the results obtained SO meagre and indefi- 
nite, that the report, in this respect at least, is almost valueless. In 
comparison with the motor tests for the localization of a cortical lesion, 
sensory tests will probably always remain less efficient. The variation 
of the persona] equation .done is enough to shake one's confidence in 
sensory symptoms; and to properly perform these tests there must be 
exercised an unusual amount of patience, shrewdness and insight into 






720 THE NON-NEURONIC DISEASES 

human nature. The instruments of precision must be employed in 
every conceivable manner and frequently at most unexpected moments. 
Unlike the testing for paralysis, we are here made to rely almost solely 
upon the patient and his subjective feelings. Hence we must study 
closely the patient's idiosyncrasies and peculiar temperament, and make 
due allowance for his past experiences and present intellectual status. 
His entire physical condition must at the same time be taken into 
consideration, for if there be a paresis present, for example, a sensory 
response may be very materially modified by the inability of the muscles 
to act and manifest the appropriate motor response. 1 have known of 
erroneous sensory diagnoses being made just in this way. 

Notwithstanding all these difficulties and drawbacks, it is ex- 
tremely desirable that every case of paralysis be carefully and accurately 
examined for general sensation ; for our knowledge of the location of 
the sensory centers is at the present day much less definite than that 
of the motor centers. Moreover, the experiments of the laboratory 
seem to favor the view that the sensory areas of the cortex are sep- 
arate and distinct from the motor areas, while clinico-pathological 
data intimate that they are identical, or at least are partly coincident. 

As long ago as 1888, and as recently as 1894, Dana contributed 
two valuable and exhaustive studies upon the relationship of the motor 
and sensory areas. Basing his arguments and proofs upon laboratory 
experiments and clinical observations, he concludes that injuries and 
destruction of the motor cortex are accompanied by disturbance of 
cutaneous and musculo-articular sensations. He holds that the -motor 
cortex is essentially motor, not sensory in the way that Bastian holds 
it to be. The parietal lobe is the great seat of sensation, but the motor 
cortex is a "sensory-memory-motor organ." 

On the other hand, Mills reiterated in 1902 what he stated in 
1898, that he believed in the separate localization in the cerebrum of the 
representation of sensation and of movements. 

In regard to the location of the centers for cutaneous sensations — 
touch, pain, temperature and even the sensation commonly known as 
the "muscular sense" — many views have been advanced. The general 
consensus of opinion holds that the optic thalamus is the basal ganglion 
for the reception of sensory impulses from the outer world. Luys, 
Ferrier, von Monakow, Foumier and Crichton Brown so taught, though 
Flourens, Longet, Tamburini and Scruff attributed motor functions to 
the ganglion. Above the thalamus the sensory paths radiate through 
the corona and terminate chiefly in the cortex of the parietal and tem- 
poro-sphenoidal lobes. Below the thalamus the sensory paths are clear- 
ly distinguishable from the motor. Do these two paths so unite or 
intermingle above the ganglion as to terminate in the same cortical 
areas, or do they still remain sharply and wholly apart, one set (motor) 
going to the central convolutions, the other set (sensory) turning back 
to end in the postero-parietal lobes? 

In his earlier experiments Ferrier found that injury to the hip- 
pocampal convolution and cornu ammonis produced loss of tactile sensi- 
bility on the opposite side of the body. He therefore located the center 
for tactile sensibility in the region of the hippocampus. This was con- 



THE XOX-XEUROXIC DISEASES / 2 I 

firmed by Yeo in his experiments upon monkeys. Horsley and S chafer 
have extended the views of Ferrier, and as a result of their investiga- 
tions have concluded that the whole of the limbic lobe (including th? 
callosal and hippocampal regions) preside over the sensations of touch 
and pain, if not exclusively, at least to a very large extent. In some of 
their experiments the loss of sensation was accompanied by motor 
phenomena, which they attributed to unintentional injury to the motor 
area during the performance of the operation. As opposed to Munk 
and Scruff, who would possibly argue from this the identity, in part at 
least, of the motor and sensory areas, they state that in some of their 
experiments there was paresis of the lower limbs, with anaesthesia of 
the upper limbs, and in others anaesthesia without paralysis. There 
seems to be some very intimate connection, at all events, between the 
limbic lobe and the central convolutions ; for when we recall how fre- 
quently sensory aurae and other paraesthesiae precede and accompany 
Jacksonian symptoms produced by a limited lesion in the motor cortex, 
we are compelled to admit the extreme intimacy, if not the identity, 
of the motor and sensory areas. Many of these focal lesions do not 
extend deep enough to involve the radiating fibres from the sensory 
areas and their mutual influence must, therefore, be entirely cellular 
and transmitted from one to the other by associating- neurones. The 
influence may be merely of an inhibitory sort, for clinically the anaes- 
thesia accompanying such forms of local paralysis is never complete, 
but is rather of the inhibitory type. Brown-Sequard gave special atten- 
tion to the extensive inhibitory functions of the nervous system, and in 
the light of his investigations such an explanation is not entirely un- 
warrantable. If the sensory and motor areas were identical, it would 
he hard to comprehend how a limited focal lesion could give rise to a 
complete paralysis and incomplete anaesthesia in related parts of the 
body. Both sets of cortical cells would presumably be simultaneously 
injured and the anaesthesia would run parallel in extent and severity 
with the amount of paralysis. 

There is a suggestion in the recent observations of Sherrington 
and Griinbaum that may explain the conflict of views in regard to 
sensation as a function of the central convolutions. These experi- 
menters found in their elaborate examination of all types of anthropoid 
apes only the pre-central (ascending frontal) convolution to be motor. 
No motor response was ever obtained by stimulation of the post-central 
convolution (ascending parietal). 

Flechsig includes the post-central convolution in the tactile radia- 
tion. 

All that can be affirmed positively, then, is that the sensory con- 
ducting tract passes to a large extent into the central convolutions, 
though its sphere of radiation is to be found elsewhere, particularly in 
the parietal lobes (von Monakow). Some hold that only touch and 
muscular sense are appreciated by the central areas, while other sensa- 
tions, especially that of pain, are to he located in the gyrus fornicatUS. 
The stereognostic sense is located by von Monakow in the central areas, 
by others in the parietal ; but, as I have shown elsewhere, this is such 
■a complex sense that it can hardly he justly assigned to any one special 



722 THE NON-NEURON IC DISEASES 

area. Mills locates it in the superior parietal convolution. The parietal 
lobe is held responsible for the perception of the muscular sense by 
Nothnagel, Luciani, Mills and others, a view which has been supported 
from clinical observations by Vetter, Basset and von Monakow. As 
I have also shown elsewhere, it is not at all improbable that even here 
in regard to the muscular sense, the motor zone has come into active 
play and had much to do with the sense of position. It is to be noted 
that Charcot and Pitres doubted the sensory importance of the motor 
regions. 

In regard to the cortical visual area there is still some dispute, 
though speaking generally it may be said to coincide with the occipital 
lobe. The cuneus and the parts around the calcarine fissure (Hen- 
schen) are usually assigned as its limits. Oppenheim teaches that the 
gyrus fusiformis (lateral occipitotemporal), lingualis (median occipito- 
temporal), and first occipital convolution should probably be included. 
As everybody knows, destruction of this area causes bilateral hemi- 
anopsia of the opposite side. Total blindness follows extirpation of 
both occipital areas. Further localization of the visual conceptions of 
space, light and color is quite impossible, though there are many 
hypotheses proposed. The angular gyrus is no longer regarded as a 
center for visual sensations. The disturbance of sight which Ferrier 
and others long ago attributed to injury of the gyrus is now known 
to have been caused by involvement in the injury of the visual con- 
ducting paths that run through and near it. It has been recorded that 
lesions of the left inferior temporal lobe, the supra- marginal gyrus, 
cause alexia — inability to read — without disturbance of the ability to 
speak. 

The cortical area for the sense of smell has been localized in the 
gyrus uncinatus, as injury here has in some instances produced anos- 
mia (Hughlings Jackson). In a case of anosmia reported by Schafer 
and Frey there was atrophy of the olfactory tract and changes in the 
gyrus uncinatus and horn of ammon. The olfactory apparatus is much 
atrophied in man as compared with the lower animals. From his com- 
parative studies Edinger is led to assign the cortical areas for smell 
to the lobus pyriformis and the cornu ammonis. Professor Oiiodi, of 
Budapest, notes that in a case of cacosmia there was found a tumor 
in the right gyrus hippocampi. Hallucinations of smell have been asso- 
ciated with tumors of the gyrus uncinatus and gyrus fornicatus, though 
Edinger doubts the power of the gyrus fornicatus to perceive sensa- 
tions of smell. The cacosmia in this case may well have been a mere 
"neighborhood symptom." Hemorrhages, emboli and tumors of the 
temporal lobe have been accompanied by loss of smell, and the same 
explanation is probably applicable in these cases. 

The cortical area for the perception of taste has not yet been dis- 
covered. It is probably near and closely related to the center for the 
sense of smell. Paget believed that the perception of thirst and hunger 
was somehow associated with the basal surface of the temporal lobe. 

The center for hearing is somewhat better known, and is generally 
accepted as coinciding more or less with the upper convolution of the 
temporal lobe — that part of the convolution, according to Flechsig, 



THE XOX-XEUROXIC DISEASES 723 

which lies hidden in the fossa of Sylvius. Ferrier at first located this 
center positively in the superior temporal convolution of monkeys. The 
experiments of Brown and Schafer, however, showed conclusively that 
even when both temporal lobes were removed there was no loss of the 
power of hearing. In reply to Ferrier and Yeo, these experimenters 
remarked that they had "frequently observed that monkeys which have 
experienced no cerebral lesion whatever will sometimes fail to start or 
show any sign of hearing at the report of a pistol, whilst others will 
react very strongly to such a noise.' 7 Might not this be easily accounted 
for on the basis of the association of ideas, some monkeys having from 
their individual experience in some way become fearful of certain kinds 
of noise, while others, lacking such experience, remain indifferent to 
them? If such were the case, it would open the way for the considera- 
tion of the superior temporal gyrus as a mere psychic or memory 
center for hearing, and thus harmonize the two opposing views of 
Ferrier and Yeo on the one hand, and of Brown and Schafer on the 
other. As a matter of fact, it is now pretty generally accepted that 
the superior temporal convolution is the seat of mind audition and 
that its destruction causes ziord-dcafness, and not sound-deafness. 
This sensory aphasia literally consists of a loss of the power of recog- 
nizing word sounds and their constructive association. The victims of 
this form of aphasia are in the plight of one who is talking to a for- 
eigner whose language he is absolutely ignorant of. When such a 
patient suffers from a bilateral lesion in the superior temporal convolu- 
tions he is said to have "cortical deafness." 

In this connection it is well to remember that this psychic word- 
center is the most important of the group of centers involved in the 
production of speech. Its proximity to the island of Reil may account, 
therefore, for the fact that lesions of the island usually cause dis- 
turbance of the power to correlate the speech centers, and thus pro- 
duce such symptoms as paraphasia, lapsus linguae, defective word and 
sentence formation, etc. See further the section on the disturbances of 
language. 

Our knowledge of the motor areas of the cerebral cortex is much 
more definite, so far as their location is concerned, than is our knowl- 
edge of the sensory areas. The examination of motor manifestations, 
both in the laboratory experimentally, and at the bedside clinically, is 
susceptible of a high degree of accuracy as compared with the exam- 
ination of sensory phenomena. As a result of extensive experimenta- 
tion upon the lower animals and of clinico-pathological observation in 
man, it has come to be established that the motor zone correspond-, 
with the central convolutions on either side of the fissure of Rolando,, 
the adjoining parts of the frontal and parietal lobes, the paracentral! 
lobule, and the supramarginal gyrus. There are no known sharply 
defined boundaries to this zone. Its center or rather centers of maxi- 
mum energy seem to lie along the central convolution just in front of 
the fissure of Rolando. In comparison with both anterior and posterior 
central convolutions, the areas of the frontal and parietal lobes lying 
contiguous to them play a minor role. The experiments made recently 
upon the apes by Sherrington and Grunbaum localize the motor center 



724 THE NON-NEURONIC DISEASES 

absolutely in front of the fissure of Rolando. There was no response 
of a motor character whatever to stimulation of the post-central (as- 
cending parietal) convolution. The view is fast gaining ground that 
there are no pure motor centers behind the Rolandic fissure. The so- 
called motor areas thus indicated control each the musculature of the 
opposite half of the body. This control is not direct, but is exercised 
through certain lower deposits of gray matter. They are bilateral 
areas, therefore, and in both hemispheres subserve the representation of 
definite, and purposive movements produced by groups of muscles 
rather than the individual muscles themselves. They are the teachable 
memory areas for acquired movements. Most authorities regard them 
as purely motor in function, while others look upon them as sensory- 
motor. 

Focal lesions of these areas provoke monospasms and unilateral 
convulsions, followed by an oncoming paralysis which may vary in 
type, according to the location, character, and extent of the lesion. The 
paralysis which succeeds the spasm is more or less localized in extent 
and degree. It is of the monoplegic type, involving, however, related 
muscles that functionate in the expression of particular movements 
rather than the single muscles. If the lesion is unlateral and extensive, 
the paralysis is of the facio-brachio-crural type, a true hemiplegia. 
This paralysis is accompanied by an exaltation of the spinal reflexes. 
It always begins in the same part — or rather the spasm that precedes 
it — in different attacks, as for instance, the toes, the fingers, the face. 
The hemiplegia is not crossed, the face and body being affected on 
the same side. It is, of course, on the side opposite that, of the lesion. 
There is no direct involvement of the nuclei of the cranial nerves. 
Muscles that usually work together, as for instance, those of degluti- 
tion and respiration, and which are equally represented in both cere- 
bral hemispheres, exhibit but little paresis or else are so quickly com- 
pensated for in the unaffected hemisphere that their weakness passes 
unnoticed. The more complex and individualized the muscles are in 
their normal activity the more will they be paralyzed ; hence the upper 
extremity shows a higher degree of paralysis than the lower. There is 
no atrophy of the muscles and the electrical reactions remain normal. 
Late contractures occur in the parts paralyzed. 

In the lower third of the central convolutions, just above the 
fissure of Sylvius and embracing the lower end of the Rolandic fissure, 
are located the centers for the face, the tongue, and the upper part of 
the oesophagus. Just anterior to this center, at the posterior extrem- 
ity of the third frontal convolution, lies Broca's well-known center of 
speech, while behind it is a small area that controls the movements of 
the larynx. The larngeal muscles are rarely paralyzed as they work 
together and in lesions of one side or the other are quickly compen- 
sated for. The speech center is a bilateral center, but is only active 
apparently on the left side in right-handed people. The ri^ht speech 
center is active in left-handed people and can, by training, be made to 
compensate in some cases for loss of the left center. These centers 
are called the memory centers for the emission or motor part of speech, 
hence their disease gives rise to motor aphasia. 



THE XON-XEUROXIC DISEASES 725 

Passing upward along the fissure of Rolando, we meet seriatim 
the centers for the fingers, the hand, the arm, and the shoulder, the 
maximum points of the centers seeming to occupy especially the mid- 
dle third of the precentral convolution. 

In the upper third of the convolutions are the centers for the leg, 
the foot, the toes, and the hallux, the last being found close to the mar- 
gin of the hemisphere and even extending well over into the paracen- 
tral lobule. On account of the nearness of these marginal centers 
of both hemispheres to one another, paraplegic, better stated as diple- 
gic, conditions, are relatively frequent, as Charcot pointed out. 

Just in front of the upper part of the precentral convolution the 
great trunk musculature is said to be represented. Horsley and Shafer 
locate the trunk center in the marginal convolution. Munk believes 
that it lies in the frontal lobes, while Jackson assigns it entirely to the 
cerebellum. 

It must be remembered that all of these centers shade off into one 
another so that no sharp outline can be assigned to any one of them 
individually. They are the only cortical motor areas that can be ac- 
cepted at the present day with anything like positiveness in man. Ex- 
periments upon the monkey have indicated that these areas may again 
be subdivided and smaller areas detected for the representation of small 
and special forms of movement. Within the lower centers, for instance, 
we find clearly represented the laryngeal, masticatory and deglutitory 
muscles, though there is some discussion as to the accuracy of all of 
them in regard to certain details. Lateral movements of the head, ele- 
vation of the eyelids, and dilatation of the pupils are all represented, 
according to the observations of Ferrier upon monkeys, in the posterior 
ends of the first and second frontal convolutions. 

The visceral muscles and vasomotor system do not seem to have 
any representation at all in the cerebral cortex, though that hardly 
seems possible when we remember how the emotions affect the circu- 
lation of the face and how even the viscera are perceived at times in 
the realm of consciousness. Their bilaterality and close unity of func- 
tion, as well as the fact that all the organs of vegetative life are more 
especially under the control of the sympathetic nervous system, may 
account for the lack of their higher representation in the cortex. Some 
authorities declare that a regulating influence upon the heart and bloo 1 
vessels, upon the heat production and upon the visceral nervous appa- 
ratus is exercised in the opposite half of the body by centers located in 
and near the central convolutions. These, however, together with tin- 
centers for the bladder and rectum and for the trophic regulation of 
the musculature in general, though supposed to reside in and about the 
motor zone, are all entirely hypothetical. Certainly no symptoms in 
unlateral disease of the cerebral cortex have yet afforded us am basis 
whereon to locate or even to assume the existence of such centers. 

Those who maintain that the histological structure of the central 
convolution affords a clue to their proper function reason beyond the 
facts. Gowers says, for instance, that "it is instructive to note that in 
this part are found the largest ganglion cells met with in the cortex, 
cells comparable to, though exceeding in size, the certainly motor cells 






7^6 THE JSON-NEURONIC DISEASES 

of the anterior cornua of the spinal cord." On the other hand, we find 
in the hippocampal convolution, which is admitted to be sensory in func- 
tion, pyramidal cells very similar to those found in the central convo- 
lutions. They lie just beyond what is known as the stratum radiatum. 
Furthermore, these large cells have never as yet been absolutely proved 
to be motor. They may be muscular, in the sense that they are in 
immediate connection with the musculature of the body and capable 
of a grosser and more vigorous form of activity than are the more 
delicate receptive sensory cells. Neurones, whether of the motor or 
sensory type, are all alike in their intimate structure so far as we know, 
and their exhibition of neurility is to all intents and purposes the same 
everywhere. When we remember that sensation itself is but a mode 
of motion, we can understand that these giant-cells may differ from the 
smaller ones in degree rather than in kind. The reflex character of 
most of the sensory-motor phenomena would seem to indicate that both 
sets of neurones possess the faculty of receiving and emitting nervous 
impulses and it is hard to escape the conclusion, therefore, that the 
essential differences in their functions are the result of the nature of 
the terminal end-organs with which they are respectively connected. 
As an essential part of the neurone doctrine, it is now taught even 
more emphatically than heretofore that the terms sensory and motor 
as applied to the nervous elements have more regard to their peri- 
pheral end-organs than to their innate structure or even to their cen- 
tral connections. 

Physicists are resolving all phenomena into molecular motion, the 
differences in the phenomena into the different forms of molecular 
motion. Light, heat, electricity are but the expression of the differ- 
ent modes of movement among the molecules of matter. Nervous 
activity has not infrequently been likened to electricity, but whether 
the comparison be true or not, it is more probable that the former is 
as much a mode of molecular motion as is the latter. Chemical changes 
accompany both and chemical changes are the result of atomic trans- 
formations. Both sensory and motor phenomena, nervous as well as 
muscular, are alike the result of molecular movements. The simple 
muscular contractions are recognized as the direct expression of mole- 
cular vibrations within the muscular elements and the reflex circle, 
beginning in a peripheral irritation, running through the center from 
sensory to motor cell and finally passing out again to terminate in gross 
muscular contractions, is simply the transmission of the same molecu- 
lar disturbance, differing in degree, but not in kind, throughout the 
various parts of the arc. This is so universally accepted now by science 
that its reiteration seems almost like a truism, but for my present pur- 
pose of showing the universality of the one phenomenon needs to be 
repeated. If the reader cares to pursue this line of thought further, he 
may consult Gowers' admirable little brochure entitled The Dynamics 
of Life, in which the author most elaborately and convincingly eluci- 
dates the fact that all neuro-muscular phenomena are but the mani- 
festation of chemical phenomena and that these phenomena are hut the 
expression of atomic and molecular motion, the origin of which motion 
is to be attributed primarily, so far as we are capable of knowing, to 



THE NON-NEURONIC DISEASES 72.7 

the solar influence through light and heat. Nay, more. Even the 
higher, psychic manifestations of nerve force can be reduced by analy- 
sis to real or representative movement, even the gross muscular move- 
ments, as has been well pointed out by Romanes in his Mental Evolu- 
tion in Animals. 

The most positive knowledge we possess in regard to the functions 
of the cortex is that the central convolutions somehow preside over 
the movements of the body. And yet, as Gowers says, "We need 1101 
conceive that these parts subserve no other function (we shall pres- 
ently see reason for believing that they have sensory as well as motor 
functions)." Injury to these convolutions produces spasm or paraly- 
sis ; and so far as we know, these symptoms are not produced by cor- 
tical lesions outside of these convolutions or their immediate neigh- 
borhood. That these are not the only centers which preside over vol- 
untary movements is to be inferred from many experiments upon ani- 
mals. A rabbit whose entire cerebrum has been removed can still 
run ; and according to Goltz, there was no complete paralysis, but only 
a slight anaesthesia observed in a dog whose whole brain except one 
occipito-parietal lobe was excised. 

It is an old established fact that removal of the cerebral hem- 
ispheres, olfactory ganglia, optic lobes, corpora striata, and optic 
thalami does not eventuate in the loss of voluntary motion and gen- 
eral sensibility. There is loss of intelligence and of rational inhibi- 
tion, but the animal still executes purposive, instinctive movements 
which are quite different from the simple reflex acts depending upon 
the spinal cord. Hence arises the question, what is the nature of these 
disturbances of voluntary motion caused by the destruction of the cor- 
tical motor areas? A dog deprived of his two sigmoid gyri does not 
manifest motor paralysis, if by that term is meant absolute loss of 
motility. There is not a single physiologist who denies such an ob- 
servation ; hence the ground for the criticisms of Goltz, the distin- 
guished opponent of the localization theories. The motor areas must 
preside therefore in some special way over the muscular apparatus and 
not directly, as at first seemed to be the case. In 1876 Hitzig spoke of 
the effects of cortical lesions in the motor area as "the expression of 
an abnormal representative action;" in other words, as the result of 
a destruction of the motor images belonging to certain voluntary 
movements. The muscles of the animal are not paralyzed, but the 
animal no longer possesses the mental pictures or ideal representations 
of the movements it should make or desires to make. 

Nothnagel and Bastian favor the theory of Hitzig, but they differ 
from him in locating a center for the "muscular sense" outside of the 
central lobules. The former declared to the Sixth Congress for Internal 
Medicine, held at Wiesbaden, that he had never known focal lesions 
of the motor zone to produce loss of the muscular sense, but that such 
lesions were often accompanied by loss of the tactile sense. In a 
paper published in Medicine I suggested that tin- SO-cailed "muscular 
sense" is but a differentiated expression of the tactile sense. Noth- 
nagel places the sensory area in the parietal lobes, where he also lo- 
cates, with Seguin, the special center for the muscular sense.. Noth- 






728 THE NON-NEURONIC DISEASES 

nagel further affirms that the parietal lobes bear the same relationship 
to the central and paracentral lobules that the convolution or area of 
Broca bears to the cortical hypoglossal and laryngeal motor areas. In- 
jury to the parietal centers may produce ataxia without true paralysis, 
and injury to the central areas may cause paralysis without the loss 
of the muscular sense. This is somewhat of a return to the limitation 
views of Ferrier as originally propounded ; and, in fact, both Nothnagel 
and Charcot separate the motor areas from the centers for cutaneous 
and muscular sensibility. For Charcot, however, the cortical motor 
centers are the seat of motor representations or conceptions which 
must necessarily precede the accomplishment of any conscious volun- 
tary movement, while the muscular sense or kinsesthesic sensibility of 
Bastian is subserved by the cortical centers for sensation. 

According to Schiff, the so-called motor areas are entirely sen- 
sory ; their activity is largely of the nature of a reflex ; and the paraly- 
sis due to their destruction is really the result of the loss of tactile sen- 
sibility. Munk does not believe that these centers determine move- 
ments directly or in any sort of reflex manner, but merely by the awak- 
ening of the mental images or representations of both general sensi- 
bility and motility. These ideational centers are not in immediate 
connection with the individual muscles, nor do they exert their in- 
fluence directly for their individual activity. As Dr. Theodore W. 
Fisher tersely puts it, "The will can only control and the mind is only 
conscious of movement in the mass." The fact that stimulation of 
certain areas of the cortex produces movement of certain groups of 
muscles and eventuates in the coordinated movements of the segments 
of the limbs shows that movements, and not muscles are represented 
in the cortex. Many of the opponents of Ferrier have lost sight of 
this fact because this investigator insisted so strenuously upon the ana- 
tomical distinction and separation of the sensory and motor areas, and 
upon the sharp limitations of the latter to the central lobes. 

Munk's theory is popular in Germany and makes the so-called 
motor areas almost entirely sensory. The activity of these centers 
results in "conceptions of movements" rather than in movements them- 
selves. They are the psychical source of the impulses which farther 
down the tract (possibly in the basal ganglia or anterior cornua of 
the cord) are transformed into the true motor stimuli that set the mus- 
cles into action. The cortical motor area is therefore named by Munk 
the "Sense-sphere" (Fuhlsphare) . Gowers' objection to this theory 
is that the "sense of innervation," an element of the threefold "con- 
ception of movement," is a sense of something which is not itself sen- 
sory and which is commonly termed motor and that destruction of this 
region causes loss of this "motor" function out of all proportion to any 
demonstrable sensory loss. The first of these objections seems inade- 
quate to me; for it is a fact as Strieker and others have shown that 
movements are preceded by psychical representations, which representa- 
tions must obviously be of a sensory character. Franck inclines to 
the theory of a reflex action being the essential function of the motor 
areas. He believes that the motor, like the sensory, zones are only 
the points of departure for voluntary motor impulses while the true 



THE NON-NEURONIC DISEASES /2') 

motor apparatus or executive centers are to be found in the cellular 
elements of the medulla oblongata and spinal cord. All of the cortical 
areas, according to this author, are merely centers of voluntary asso- 
ciation. We know that the sensory and motor elements of the cortex 
are united by associating tracts, just as they are lower down in the 
cord, to complete the reflex arcs. The reflex phenomena, both spinal 
and cerebral, necessarily presuppose such a functional union of the 
sensory and motor radicles. This it seems to me is quite adequate to 
explain the occasional association of the two sets of symptoms when 
the lesion happens to be limited to one or the other area. . 

Formerly all reflex functions were supposed to belong exclusively 
to the spinal cord ; but to-day we consider the cerebral centers as much 
the centers for reflex action as are the spinal. Many of the Jacksonian 
epilepsies are undoubtedly of simple reflex origin. Mills reported a 
case in 1880, clearly Jacksonian in type, in which there had been seiz- 
ures for eleven years as the result of a fibroma in the hand. When 
the tumor was excised, the epileptic seizures ultimately disappeared. 
''In the normal brain," Mills writes, "no reflex actions can be performed 
without exciting to action secondary volitional movements, which no 
longer require the stimulating influence of a reflex action. " The ab- 
sence of gross cortical lesions in some forms of Jacksonian epilepsy, 
and Heidenhain's experiments in hypnotism, with other observations 
and facts, all prove conclusively the reflex function of the cortical areas 
of the brain. 

Franck speaks of them as psychomotor centers, because they con- 
trol by their psychical influence the true, lower motor apparatus. He 
says that "in examining the movements produced by the excitation of 
points under the control of the cerebral cortex, they may be regarded 
as analogous to reflex movements ; but the essential difference between 
the movements so started and the ordinary reflexes consists in the point 
of departure of the original impulse. In one case it is cerebral, in the 
other cutaneous ; but in every case it is peripheral in relation to the 
center of motion (medullary centers)." Strictly speaking, then, the 
pyramidal tracts transmit afferent and not efferent impulses to the 
motor cells of the cord and medulla. Marique adopts, in part, this 
reflex theory as explanatory of the functions of the cortical motor 
areas; for he found that simple separation of the motor from the 
sensory areas, as a result of cutting the associating tracts, produced 
the same form of paralysis as when the cortical motor areas themselves 
were removed. He concluded, therefore, that the motor areas could 
not act of themselves, but that functionally they were dependent upon 
the impulses transmitted to them from the sensory area- of the parieto- 
occipital region. This question is far from being settled, however, since 
Mich varying results have been obtained in the experiment- of Franck 
and Pitres, Marique, Vareth, Exner and Paneth. 

According to Soury, Lisso has collected since 1882 some eighty- 
eight cases in which there was disturbance of sensation when the lesion 
was confined to the motor area. Hence Tripier and Gilbert Ballet have 
named the cortical area the "sensitive-motor zone." Exner admits that 
the different areas for tactile sensibility of the various parts of the 



73° THE NON-NEURONIC DISEASES 

body are closely intermingled with the motor areas. In his study of 
aphasia, Dejerine says : "These disturbances of cutaneous sensibility 
accompany the beginning of the paralysis itself in the majority of cases ; 
sometimes they even precede the latter. These phenomena are not rare 
in the course of a hemiplegia of cortical origin and they deserve close 
study." The lesion in Dejerine's case was confined exclusively to the 
motor cortex, leaving the sensory paths intact. Dupuy notes that 
Horsley reported to the Congress of Brighton, in 1886, that the removal 
of a part of the motor cortex in three patients for epileptoid seizures 
symptomati® of cortical lesions resulted in the partial or complete loss 
of sensibility. Seguin and Weir reported the case of a man, aged 
thirty-nine, who complained in the autumn of 1882 of severe head pain 
and convulsive attacks limited to the right side of the neck and face. 
From 1885 these attacks occurred very frequently and were associated 
with a sensation of cold. The spasms involved the right arm and hand 
as well as the face. Finally paresis supervened in these parts and was 
accompanied by aphasia and agraphia. The diagnosis was tumor in 
the facial center of the left motor zone. Operation proved it to be a 
sarcoma, about an inch in thickness, nesting beneath the foot of the 
second frontal and the anterior border of the ascending frontal convo- 
lutions. A report of the case in the Journal of Mental and Nervous 
Disease, December, 1888, one year after the operation, states that there 
was unquestionably anaesthesia of the cheek, hand and forearm to 
contact tests as well as with the aesthesiometer. There was also anaes- 
thesia of the lower part of the face, lips and inside of the cheek. From 
the study of the sensory tracts and of a series of American cases of 
cortical lesion, Starr came to the conclusion that the motor and sensory 
areas coincided, though the latter extended beyond the former and in- 
cluded the postero-parietal lobe as well as the Rolandic region. Four 
of the cases in Starr's list belonged to Mills, and in reviewing his notes 
the latter came to the conclusion that they at least did not support the 
inference drawn by Starr. From a careful review of one hundred 
and thirty-seven cases, Dana decided that the sensory (tactile sensa- 
tion) and motor areas were coextensive. In the discussion of Dana's 
paper, Starr and Seguin argued with the author, while Mills favored 
the teaching of Ferrier — namely, that the center for tactile impressiini> 
is to be found in the gyrus fornicatus and gyrus hippocampi. Sher- 
rington and Grunbaum's experiments tend to negative the idea that 
the gyrus fornicatus is concerned with common sensation. 

Strieker maintains that motion and sensation are so intimately re- 
lated that they are almost identical. His views may be portrayed most 
clearly by means of an illustration. When one represents to himself, for 
instance, the movements of a cloud, the muscles of the eyes underg > 
the same sort of a sensation as though they were actually gazing at a 
moving cloud. By checking this muscular sensation within the eyes, 
the mental image of the cloud immediately ceases its movement. The 
cloud seems absolutely stationary. 

Among die Italians. Lussma and Lemoigne maintain that there are 
sensory and motor areas in the cerebral hemispheres, but that they do 
not act upon one another after the manner of a simple reflex. Tarn- 






THE NON-NEURONIC DISEASES . J$ I 

"burini, Luciani and Seppilli have elaborated since 1876 the theory thai 
the "motor zone" consists, en the one hand, of the center for cutane- 
ous and muscular sensibility and, on the other, of the centers for motor 
ideations. This, it will be recognized, is a very elaborate, mixed and 
comprehensive hypothesis. It well illustrates, says Soury, the eclectic 
tendencies of the Italian school. As a general rule the Italians are 
as much opposed to the views of Hitzig and Xothnagel as they are to 
those of Schiff and Goltz. They lean somewhat toward the theories of 
Ferrier and his English followers. In other words, they believe that 
the paralysis caused by injury of the cortical motor areas, pathological 
or experimental, is neither ataxic nor reflex. It is decidedly and en- 
tirely a paralysis in the truest sense of the word. Such at least seems 
to be the opinion of Albertoni and Michieli, Lussana and Lemoigne, 
Tamburini, Luciani, Seppilli, Maragliano, Bianchi, Palmerini, Ton- 
nini and others. In the language of Maragliano, all motor phenomena 
should be regarded ''as dependent upon true voluntary motor centers, 
which are capable, without the intermediation of any other motor cen- 
ters, of starting into activity the muscular apparatus of the body." 
Equally concise and clear in their statements are Luciani and Tam- 
burini. These authors, unlike Ferrier, locate even the centers of vol- 
untary motion in the basal ganglia, especially the corpora striata. 
Injury to these ganglia as well as to the corresponding centers of the 
cortex does not result in ataxia, or in the phenomena of incoordination ; 
nor is any alteration of general sensation to be detected in animals 
whose motor zones have been operated upon. The striate body, it 
will be remembered, is, according to Ferrier, the general center for 
movements which were once voluntary but which have afterward be- 
come automatic. Thus a dog can still run and swim if the striate body 
is left intact, though the corresponding cortical areas may have been 
removed. Luciani and Tamburini endow the basal ganglia with the 
same pyschic functions possessed by the cortical areas and thus differ 
considerably from Ferrier. They speak of them as psychomoter cen- 
ters, probably meaning thereby that the basal ganglia as well as the 
cortical areas are in direct connection with the sensory centers. "The 
basal ganglia," they say, "and especially the corpora striata, poss 
the same physiological value as the centers for voluntary motion do; 
or, in other words, these centers can be put into action directly by 
psycho-sensitive sensorial processes." When these authors promul- 
gated the above-mentioned ideas, it was supposed that the function of 
the striate bodies was motor; now, however, it is known that the hemi- 
plegias which result from hemorrhage in this region are caused by 
the injury done to the internal capsule. In fact, the striate' bodies have 
teen transformed completely into cysts without a paralysis occurring 
so long as the internal capsule remained untouched. Hence these earlier 
views of Luciani and Tamburini are now regarded as quite untenable. 
Nevertheless, it must be admitted that the recent study of the striate 
bodies (caudate nuclei) especially by Baginsky and Lehmann seems to 
demonstrate that there was a modicum of truth in the earlier views of 
these Italian authors. 

The so-called paralysis which results from a destructive lesion of 



732 THE NON-NEURONIC DISEASES 

the excitable zone of the cerebral cortex is believed by some of the 
Italian investigators to be due entirely to a loss of sensation. Silvio 
Venturi, of Padua, adopted this ataxic theory as far back as 1878. It 
was Schiff, the distinguished predecessor of Luciani in the chair o£ 
physiology at Florence, who became the chief exponent of this sen- 
sory explanation of the paralysis. In 1871, the year after the experi- 
ments of Fritsch and Hitzig, the editor of L'Imparziale medico, in- 
spired by Scruff, wrote that all the immediate effects of injury to the 
so-called motor centers of Hitzig were really the result of a disturbance 
of sensibility and were limited entirely to that sphere. In several Flor- 
entine publications, issued in 1873 and 1876, Schiff recalls these facts. 
According to this physiologist, a dog with a cerebral lesion is not 
affected with any loss of energy in the muscles of the opposite half 
of the body, but merely with an absence of the feeling of surety and 
power of adjustment in its various movements because of the loss of 
tactile sensibility. The general movements of leaping and running are 
all well performed, but there are marked evidences of an uncertainty 
in regard to the position of the limbs. This anaesthesia is entirely cuta- 
neous, according to Schiff, while the sensibility to pain and pressure re- 
mains unaffected. Alterations of the sense of pressure and of tempera- 
ture are caused by the increased depth of the cerebral mutilations.. 
While these views, together with the experiments of Schiff, are not 
accepted by the majority of physiologists, they have had their influence 
in greatly modifying the original theories of many in regard to the 
motor character of the so-called motor areas. Hitzig himself, who 
was so vigorous an upholder of the purely motor theory, has altered 
his conceptions to such an extent as to refer to these motor phenomena 
under the name of disorders of the muscular conscience. Schiff's. 
theory is that of a pure reflex. An impulse from the periphery is sent 
inward to the brain and there within some hitherto undiscovered sub- 
cortical centers it is transmuted into an efferent impulse which is sent 
out again to the muscular apparatus. This cerebral reflex, he insists, 
is similar to the spinal reflex and the phenomena due to its disturb- 
ance are similar to the reflex phenomena due to injury of the posterior 
columns of the cord. It should be observed that Schiff locates the re- 
flex centers, not in the cortex itself, but somewhere beneath the cor- 
tex. Von Monakow holds that all bilaterally acting muscles, such as- 
those of respiration, deglutition, and mastication are innervated from 
some unknown subcortical centers that vary slightly, if at all, from 
the cortex. There have been many objections and objectors to these 
views of Schiff and his following in regard to them is quite small. It 
must be admitted, however, that, like his opponent, Hitzig, he has done 
valuable service to the science of cerebral localization ; for if Hitzig 
discovered the results of injury to the motor areas of the cortex, Schiff 
revealed those due to injury of the centers for tactile sensation. To 
judge from the doctrines of Munk, Luciani and Seppilli, the future 
will have to acknowledge Schiff, as well as Hitzig, as one of its fore- 
runners. When Schiff asserts that "one thing is positive, there are 
no cortical centers," we are somehow forcibly reminded of Goitz. 
Though the former enumerated many objectors, chiefly among the 



THE N0N-NEUR0N1C DISEASES 733 

followers of Ferrier, such as Lussana, Tamburini, Bechterew and Hors- 
Jey, his teachings have acted as a wholesome check upon the too rapid 
assumption that all movements of the body originate from certain lim- 
ited areas of the cerebral cortex. They have induced experimenters 
to study somewhat more minutely the character of all muscular move- 
ments, the relation of the centers for this movement to the centers for 
.sensation, and the influence, if there be any, of the higher mental fac- 
ulties, the purely psychic functions of the brain. 

Tamburini has attempted a reconciliation of the two opposing 
views just described. He admits it is probable that the points of the 
cortex where the inpouring sensory impulses are transformed into out- 
going motor impulses correspond identically with the cortical areas upon 
which so much study has been expended. In his own words, "Each of 
these centers may be at the same time the focus for the reception and 
perception of the sensory excitations sent inward from a given part 
of the body and the point of departure for the voluntary centrifugal 
impulse going to the muscles of the same part.'' This, he believes, ex- 
plains the absence of sensibility in the direct production of localized 
movements ; for in the one instance the electric current takes the place 
of the nervous current or impulse and in the other the removal of the 
cortical centers must necessarily abolish the perception of the peripheral 
impressions. In conjunction with Luciani, Tamburini has extended 
the same theory in regard to the excito-motor zone of the cortex to the 
centers for sight and hearing. The movements of the ear and eye- 
ball, initiated by a sensory impression at the periphery, are not of the 
nature of a pure reflex, as Ferrier believes, but simply the result of 
the intermingling of the corresponding sensory and motor elements of 
the cortex. In other words, corresponding sensory and motor cells lie 
in close juxtaposition within the various cortical areas. These views of 
Tamburini seem to be supported by an anatomical as well as by a phys- 
iological basis ; for, as 1 have already pointed out, the region of the 
hippocampus major, which Ferrier and his followers assert is sensory 
in function, contains a row of large pyramidal cells between the medul- 
lary center and the so-called stratum radiatum. These cells are iden- 
tical, so far as their microscopical appearances are concerned, with the 
supposed motor cells of the central convolutions and anterior horns of 
the cord. 

In this connection it is interesting and suggestive to note Flechsig 
thinks that for every sensory path (corticopetal) there is a correspond- 
ing motor (corticofugal) path. For instance, beside the auditor v 
myelogenetic area in the first temporal convolution, there is a cortico- 
fugal area or radiation which he believes is motor, though this has not 
yet been demonstrated. And so on for all the sensory motor couplets 
which, taken en masse for the entire brain, make up his primordial 
zones or regions of early development. 

In 1880 Luciana, who, like Scppilli. found that the effects of a 
circumscribed lesion within the motor zone of the cortex were not only 
paralysis or paresis, but also ;> more or less pronounced alteration of 
the muscular and cutaneous sensibility, wrote that "the motor centers 
and the sensory centers, which together perform a very complex func- 



734 



THE NON-NEURONIC DISEASES 



tion, are intermingled or lie in the closest proximity (in gran vicinanza) 
within the cerebral cortex." He verified the phenomena described by 
Munk, but he did not look upon the paralysis as psychical in character ; 
that is, as the result of the loss of mere sensation of mental images or 
psychic representations. It was purely organic and depended directly 
upon the injury to the motor cells, just as the disturbed sensibility de- 
pended upon the injury to the neighboring sensory elements. The mo- 
tor centers, therefore, like the centers for sight and hearing, were of a 
complex nature and in reality were sensory-motor. Luciani says, "the 
motor centers are not localized within the cortical area, called up to 
the present time 'the motor zone,' a name which we must hereafter 
abandon, since this zone is not exclusively motor. All the various re- 
gions of the cortex are more or less strewn with special motor centers. 
In order to be positive of having destroyed all the motor centers, one 
must remove the entire cerebral cortex." This is a remarkable state- 
ment of a singularly comprehensive theory, and leads us -back once 
more to the vigorous contentions of the school of Goltz and somewhat 
to the teaching of Flechsig. 

Danillo has demonstrated that when the occipital lobe, which is 
supposed to be entirely sensory in function, is stimulated, the move- 
ments of the eyes are not simply reflex, as Ferrier believed, because 
they are still observed when after the ablation of the entire cortex of the 
occipital lobe the underlying white substance is electrically excited. In 
this white substance, therefore, there must be motor fibres springing 
directly from the cortex of the occipital lobe, unless we imagine that 
these same fibres go to the central lobules and through them, rather 
than directly, transmit the motor impulse to the muscles of the eye. 
Even such an hypothesis, however, would represent the process within 
the occipital lobe cortex as reflective, but the outgoing impulse in such 
a case would be transmitted into an ordinary motor one before it finally 
reached the eye muscles. 

Bechterew finds that when the so-called motor areas of the cen- 
tral lobules are separated from the occipital centers, stimulation of the 
latter still gives rise to the same muscular response. He argues, fur- 
thermore, that the movements of these muscles cannot possibly be of 
the nature of a simple reflex, because they are always uniform and 
localized within the same group. Stimulation of the occipital cortex 
excites motor points therefore that do not belong to the so-called motor 
zone whose fibers pass only through the pyramidal fasciculi of the 
cord. These mixed centers being thus situated outside of the cor- 
tical areas to which the pyramidal fasciculi run require for their ex- 
citation a much stronger and longer current ; their destruction does not 
involve manifest disturbances of motion ; and the movements which 
they give rise to are not very clearly differentiated from those caused 
by excitation of the true motor zone. Bechterew reasons that the sen- 
sory areas do contain motor centers, or at least motor elements, and 
he accounts for the fact of their stimulation requiring a stronger cur- 
rent and one longer in duration on the ground that they do not connect 
with their corresponding muscles through the intermediation of the 
anterior roots of the spinal cord, but through certain masses of gray 



THE NON-NEURONIC DISEASES 735 

matter situated deeply within the cerebral hemispheres, probably the 
optic thalami. According to Bechterew, then, there are two sorts of 
motor centers within the cerebral cortex. One variety is easily ex- 
citable and is found in the central convolutions ; the other is not so 
easily excited and is scattered in among the sensory centers. This au- 
thor bases his views chiefly upon his experiments on new-born animals, 
in which the movements of the ear and the conjugate movements of 
the eyes can only be produced by direct stimulation of the correspond- 
ing areas of the cortex one week and one month respectively after the 
movements of the limbs have been elicited by excitation of the central 
convolutions. It is not to be doubted, therefore, that the sensory areas 
of the cortex contain some motor elements and exercise some special 
influence over the associated muscular apparatus. From this rapid 
review of the modern theories current among the English and Con- 
tinental physiologists, we note clearly that there is a growing tendency 
to believe that the motor centers of the central convolutions have sen- 
sory elements more or less intermingled with them. 

Thus far I have discussed only the localizations, so far as they are 
known, in the cerebral cortex ; but these do not by any means include 
all of the localizations in the brain. The functions of the basal ganglia, 
the arrangement of the projection tracts especially as they course 
through the internal capsule and the functions of the cerebellum are all 
sufficiently known to afford some clue as to the location of lesions in 
these parts. 

As the white matter of the hemispheres consists of association, 
commissural and projection tracts, a lesion within them cannot be 
sharply diagnosticated and distinguished from a lesion of the cortical 
areas with which they are connected. From the standpoint of surgery, 
it is extremely desirable to be able to distinguish a cortical from a sub- 
cortical lesion and even if possible the depth of the subcortical. Not 
many lesions are entirely and completely cortical, and many of those 
which are often supposed to be cortical are discovered upon post mor- 
tem to be subcortical. Tumors of the centrum ovale usually give rise 
to more extensive symptoms than do those of equal size in the cortex. 
Tn other words, the nearer the lesion is to the cortex the more likely 
it is to produce spasm and paralysis or paresthesia and anaesthesia in, 
for instance, the arm, the leg, or a part of the face, while on the other 
hand the farther it is away from the cortex, as, for instance, in the 
internal capsule, the more likely it is to provoke a hemiplegia or a hem- 
ianesthesia. The spreading out of the tracts above the capsule explains 
clearly enough the reason why cortical lesions tend to produce mono- 
plegias and subcortical more extensive paralyses. Though not abso- 
lutely reliable, this distinction is an important and valuable one. Seguin 
made a careful study of the differential signs between the cortical and 
subcortical tumors, and in a general way concluded that cortical lesions 
produced "localized clonic spasm, epileptic attacks beginning with local 
spasm, followed by paralysis; early appearance of local cranial pain 
and tenderness; increased local cranial temperature;" whereas sub- 
cortical lesions gave rise to "local- or hemi-paresis followed by spasm ; 
predominance of tonic spasm: absence, small degree or very late ap- 



736 THE NON-NEURONIC DISEASES 

pearance of local headache and of tenderness to percussion ; normal 
cranial temperature." 

Among the subcortical lesions those of the internal capsule are of 
special significance. On account of the course of the middle cerebral 
artery, hemorrhage into the internal capsule or its immediate neigh- 
borhood, the corpora striata and optic thalami, occurs more frequently 
than it does into the centrum semiovale or on to the cortex. Usually 
the extravasation of blood causes such an extensive destruction of 
tissue that a localization diagnosis is quite out of the question; and 
even were the focal lesion in the internal capsule to be so small as ta 
confine its deleterious influence to only certain of the tracts passing 
through it, a diagnosis intra vitam between capsular and cortical dis- 
turbance would be often impossible and always extremely difficult. To 
attempt a localization diagnosis of a diminutive lesion within the cap- 
sule, one must know clearly the relative positions of the various tracts 
that run through it. The anterior two-thirds of the posterior limb of 
the capsule are occupied by the projection tracts from the motor areas 
of the cortex. These fibres hold approximately the same relative posi- 
tion to each other that the areas of the cortex do among themselves ; 
that is, beginning at the knee of the capsule and passing backward, 
we meet the face, arm and leg tracts, which, however, are not sharply 
defined, but blend with each other at the line of separation. Horsley, 
Beevor, and others have located the bundles of fibres for the glossal, 
masticatory, and laryngeal muscles in the knee of the capsule. Von 
Monakow says that the speech path positively passes through the cap- 
sular knee. When this part of the capsule only is involved in a lesion, 
there occurs paralysis of the inferior branch of the facial nerve and of 
the hypoglossal of the opposite side. If the disease is upon the left 
side disturbance of the speech will also occur. In the posterior third 
of the posterior limb of the capsule course the sensory projection tracts 
that terminate in the cortex, those from the visual areas of the occip- 
ital lobe being the farthest behind. In the anterior limb of the capsule 
is to be found the fronto-pontile tract of Brissaud, about which, how- 
ever, there is still much diversity of opinion. Injury to this anterior 
limb causes no definite localizing symptoms. With this picture of 
the internal capsule in the mind, the diagnostician might attempt a local- 
ization of a small lesion, but, as I have indicated above, he could 
not feel sure of the correctness of his diagnosis. Usually a lesion of 
the capsule is so large and destructive that the accompanying paralysis 
assumes the form of a total hemiplegia, the well-known faciohypo- 
glossal-brachio-crural type, of the opposite half of the body. With 
this hemiplegia is associated more or less hemianesthesia. 

The following symptoms are supposed to indicate tumor of the 
corpus callosum : General symptoms of brain tumor such as head- 
ache, etc. ; gradual hemiplegia followed by paraplegia ; great mental 
clulness ; sleepiness ; stupidity ; indifference to the external world and 
a low, inanimate condition generally ; absence of the cranial nerves ; 
terminal coma and death. There is much doubt about all this, however, 
as the symptomatology is so general and includes so much that is in- 
dicative of tumor of the ventricles. A definite localization of the lesion 



THE NON-NEURONIC DISEASES 737 

is therefore extremely difficult if not quite impossible. The bilaterality 
of the paralysis and its irregular type, when taken in conjunction with 
the mental deterioration and general signs of intra-cerebral tumor, are 
highly suggestive, but hardly much more. In Schuffer's collected 
twenty-live cases of tumor of the corpus callosum, ten exhibited optic 
neuritis, while in seven it was absent. Headache was wanting in 
fifteen. In all of the cases there was a change in the mentality, in- 
cluding weakness of the intellect and memory, somnolence, etc. Con- 
vulsions occurred in eleven. Disturbances of sensibility were exceed- 
ingly rare. Mental changes are more constant with tumors of the cor- 
pus callosum than with tumors in other parts of the brain. When 
such mental changes are unaccompanied by any definite localizing 
symptoms, a tumor of the corpus callosum ought always to be 
thought of. 

Complete destruction of and focal lesions within the corpora 
striata do not give rise to any definite localizing symptoms. The old 
idea that the caudate nucleus has something to do with the automatic 
movements of running, walking, etc., and that the lenticular nucleus 
(globulus pallidus) is associated with the sensory paths is not well 
established. Lesions of these bodies only reveal themselves when they 
cause paralysis by pressing upon the internal capsule. There are no 
symptoms with small, inherent lesions. 

The optic thalami are clearly in close relationship with the gen- 
eral and special sensory areas of the cortex. The expression of the emo- 
tions is somehow connected with these ganglia, for when they are in- 
volved in cases of cerebral paralysis, the involuntary manifestation of 
delight, joy, sorrow, disgust, etc., seems to be impossible. The psychic 
reflexes such as laughing and crying, are disturbed. Lesions of the 
posterior part oi the thalami, namely, the pulvinar, cause partial blind- 
ness, though this is not absolutely certain. A tumor of the pulvinar and 
adjacent parts will produce a hemianopsia which may be distinguished 
from a hemianopsia of occipito-cortical origin by the hemiopic pupillary 
reaction, since these primary visual centers control the movements of 
the pupils through the third nerve. Disturbances of hearing, taste, 
smell, and the tactile and general muscular senses have all been attrib- 
uted to disease of the optic thalami, but none of them have been posi- 
tively established. Modifications of coordination and even general 
muscular atrophy on the opposite side of the body have also been seen. 
It is obvious that as the optic thalami are closely connected with the 
corresponding cortical centers, a differential diagnosis between a thala- 
mic and a cortical lesion is quite impossible. In a case of a lesion con- 
fined solely to this ganglion, reported by Hunter, there was as usual 
a loss of the senses of smell, of sight, of hearing and of touch; the 
woman sank gradually and remained a stranger to all external im- 
pressions. The extensive character of these symptoms would of course 
suggest a basal rather than a cortical lesion, but even in such a case 
it would be difficult to say just how much of this symptomatology was 
due to pressure upon the internal capsule rather than to injury to 
the thalami. , In spite of our fairly accurate knowledge of the anatom- 
ical connections of the basal ganglia, we know very little about the 



738 THE NON-NEURONIC DISEASES 

functions of this part of the brain. Though Bechterew regards these 
ganglia as reflex organs controlling the muscular apparatus by means 
of both centrifugal and centripetal fibers, and though he, with Xoth- 
nagel and Brissaud, looks upon the optic thalamus as a center for the 
involuntary automatic movements, the subconscious, non-volitional 
psycho-reflexes of the body, his views are still largely hypothetical. In- 
voluntary movements have been observed in disease of the thalamus, 
and Nothnagel has shown that the same cause will give rise to a 
crossed paralysis "observed only in laughing while the nerve still obeys 
the will" (Oppenheim). Still more questionable than all this are the 
views of Bechterew, Scruff, Lussana, Sinkler, and others that the 
cardiac, gastric, intestinal, sexual, vasomotor, secretory and trophic 
centers are located in the optic thalamus. In a word then, the basal 
ganglia do not at the present day present any definite localizing symp- 
toms, and granting that they did, it would scarcely be of much practical 
value to us beyond the making of a diagnosis excluding the cortex, for 
these ganglia are not amenable to surgical interference. 

The anterior corpora quadrigemina, together with the external 
geniculate bodies and puhinar, constitute the , primary centers for 
sight. The geniculate bodies seem to be the chief terminus of the 
optic fibers, and in this respect are closely associated with the pulvinar. 
Bechterew alleges as a result of his experiments that lesions of the 
anterior quadrigeminal bodies produce blindness, but this has not been 
observed in man. Their relationship to the pupillary reflex and ciliary 
muscles (Henschen, von Monakow) is still problematical. Stilling be- 
lieved that some of the fibres of the optic tract could be traced to the 
corpora subthalamic a, but in regard to this there is no certainty. No 
localizing symptoms are known in connection with Lilys' body, though 
much is said about its role in the maintenance of equilibrium and of 
coordination. The same is said, however, of the corpora quadri- 
gemina, the geniculate bodies, and pretty nearly all the basal ganglia, 
all of which brings to mind the words of Foster, who, when comment- 
ing upon the interpolation of ganglionic masses in the course of a con- 
tinuous tract, such, for instance, as the optic tract, says : "All day 
long and every day, multitudinous afferent impulses from eye and ear 
and skin and muscle and other tissues and organs are streaming into 
our nervous system. . . . By the checks and counterchecks of 
cerebral and spinal activities all these impulses are drilled and mar- 
shaled and kept in orderly array till a movement is called for ; and thus 
we are able to execute at will the most complex bodily manoeuvres, 
knowing only why and unconscious or but dimly conscious how we 
carry them out." 

The posterior corpora quadrigemina and internal geniculate bodies 
are usually given the function of controlling the reflex movements 
associated with hearing. Von Monakow is not fully satisfied that the 
internal geniculate bodies have anything to do with audition. Fibres 
from the cerebellum enter both the posterior (|uadrigeminal tubercles 
and the internal geniculates, so that one of the signs of lesion in or 
near them is disturbed equilibrium. Beyond this we know of no symp- 






THE XOX-XEUROXIC DISEASES 739 

toms that are produced by focal lesions limited solely to the corpora 
quadrigemina and geniculate bodies. 

The red nucleus of the tegmentum belongs to the cerebellar sys- 
tem, and therefore subserves in part the maintenance of equilibrium. 
The nucleus dentatus, the olivary body, the red nucleus, and the gray 
matter of the pons all bear a general relationship to the cerebellar cor- 
tex the same as the corpus striatum and the optic thalamus do to the 
cerebral cortex. They all connect ultimately with the anterior horns 
of the cord. No special localizing symptom can therefore be assigned 
to the red nucleus. 

Lesions of the corpora mamillaria are not known by any localiz- 
ing signs. 

Tumors of the hypophysis or pituitary body, especially of the ante- 
rior part of it, are so often associated with the general symptomatology 
of acromegaly that they have almost come to be regarded as the cause 
of this disease. Histological structure and embryological development 
both demonstrate that the anterior part of the pituitary body is a glan- 
dular organ rather than a part of the cerebrum, a fact which might 
explain in part the relationship between it and acromegaly. In the 
Revista sperimentale di freniatria, 1892, is a report of the results of the 
destruction of the pituitary gland in thirty experiments upon dogs and 
cats. Complete destruction proved rapidly fatal ; partial destruction, 
less rapidly. The animal was profoundly prostrated and exhibited a 
change of character. There was muscular weakness with clonico-tonic 
convulsions. The breathing became difficult. Anorexia alternated with 
bulimia. Alkaline polyuria was present, accompanied by polydipsia, 
depressed temperature, and emaciation out of all proportion to the 
anorexia. The inference was drawn that the destruction of the gland 
eventuated in the formation and accumulation of some special toxic 
substance within the organism. The localizing symptoms of slow dis- 
ease in this gland are therefore neighborhood symptoms, acromegaly 
and some other signs of general emaciation. Among the neighbor- 
hood symptoms that should be closely studied in suspected tumor are 
such as are referable to involvement of the optic chiasm, the circle of 
Willis, and the structures in and about the third ventricle. 

Lesions of the epiphysis or pineal gland can only be suspected from 
neighborhood symptoms which point to implication of the optic thalami 
and the parts about the midbrain. Such symptoms, however, are usu- 
ally too general to be of any very great value in making a localization 
diagnosis. 

Focal disease of the crura cerebri is rare, but when present may 
be recognized by a hemiplegia and possibly a hemianesthesia. There 
is no way, however, of distinguishing such a lesion from one involving 
the corresponding motor and sensory areas of the cortex, except by re- 
membering that the sensory-motor area is much more confined in the 
crura than in the cortex, and hence will exhibit a more widespread set 
of symptoms with the same-sized lesion. In tumor of the crura, fur- 
thermore, the third nerve will in all probability be implicated, giving 
rise to a "crossed paralysis," hemiplegia alternans. In this form of 
hemiplegia the degeneration occurs in the central neurone for the body 



7 4 o 



THE NON-NEURONIC DISEASES 



and the peripheral neurone for the eye ; therefore the body muscles ex- 
hibit a spastic form of paralysis while those for the eye are affected 
with a flaccid paralysis and degenerative atrophy. 

The localization of lesions in the pons and the medulla is largely 
a matter of remembering the location and arrangement of the cranial 
nerve nuclei. Symptoms showing an involvement of the pyramidal 
tracts are the principal ones in pontile lesions. Tumors of the pons 
often cause conjugate deviation of the eyes, which, unlike the same 
symptom when produced by cerebral disease, is in a direction away from 
the side of the lesion. Especially true is this of tumors lying near the 
cephalic border of the pons. Lesions lying above a horizontal line 
drawn roughly through the points of emergence of the trigeminal 
nerves cause a hemiplegia and facial paralysis on the opposite side of 
the body, also a probable involvement of the third nerve. Lesions be- 
low this line produce a hemiplegia of the opposite side of the body and 
paralysis of the same side of the face. This facial paralysis is central 
and must be distinguished from that caused by disease of the facial 
root fibres or nuclei. The electrical reactions will not be those of a 
peripheral paralysis ; the paralysis itself will be more or less incom- 
plete, though more pronounced, than a paralysis due to a lesion of 
the facial tract higher* up in the pyramidal paths or in the cortex. 
Tumors upon either side of the pons which encroach upon the peduncles 
give rise to forced movements of the body, the movements being either 
toward or away from the seat of the lesion. Vasomotor phenomena, 
such as pallor, flushing, temperature changes, mucous hemorrhages, 
and epistaxis, have all been attributed to disease of the pons. Disturb- 
ances of hearing and of taste have been observed by Mills in disease of 
the lateral aspect of the pons. Vertigo, ataxia, and trismus may even 
occur as irritative symptoms of pontile lesions. 

Most authors declare that no known symptoms result from lesions 
in the lateral lobes of the cerebellum. All localizations in this part of 
the brain are referred to the middle lobe or vermis. Disease of this 
lobe is supposed to be indicated by disturbances of equilibrium, forced 
movements, and a peculiar gait known as cerebellar ataxia. Such is 
the teaching of Nothnagel. It should be remembered, however, that 
in the middle lobe decussate all the tracts that course from all parts 
of the cerebellar cortex, and that it may be these tracts that are 
especially affected in disease of the vermis. Kuh says he has seen a 
case in which an angeio-sarcoma had almost totally destroyed the mid- 
dle lobe, and yet there never was any indication of incoordination. 
Mills does not regard the cerebellum in any part as a latent region. 
In tumors of the lateral lobes the general symptoms of an encephalic 
growth receive a special cerebellar stamp. The vomiting, vertigo, and 
optic neuritis, which is more frequent in cases of cerebellar tumor than 
of tumors elsewhere in the encephalon, are more or less increased and 
are accompanied by signs of compression upon the neighboring parts 
of the medulla and corpora quadrigemina. Most of the symptoms 
attributed to cerebellar disease are really pressure symptoms. The ver- 
tigo, vomiting, and headache can only be considered as valuable local- 
izing signs by exclusion of other parts o\ the brain. Incoordination, 



THE NON-NEURONIC DISEASES 741 

vertigo, and dysarthria, or scanning speech, are the only symptoms 
that may be said to more or less definitely indicate a cerebellar lesion. 
With these nystagmus and occipital headache are highly suspicious. 
Jackson and Russel have credited the cerebellum with a special influ- 
ence upon the great trunkal muscles, but this is probably due in part 
to its general coordinating function. On account of the wide connec- 
tion of this part of the brain with almost all the other parts of the en- 
cephalon above and the spinal cord below, the general function of it 
is believed to be that of securing the . higher automatic and psycho- 
reflex movements. Even its great function of maintaining the equi- 
librium is in all probability due to its relationship to the eighth or 
space-sense nerve. The wonder, therefore, is that the localizing symp- 
toms in connection with the cerebellum are as definite as they are. 

According to Bechterew, the olivary bodies subserve the function 
of coordination, the impulses reaching the cerebellum by way of the 
decussating cerebello-olivary tract. No known localization symptoms 
have as yet been attributed directly to the olives. According to the 
same authority, the superior olives act* as a reflex center for correlating 
the movements of the head and eyes with auditor)' impressions. 

A consideration of the localizing symptoms in connection with the 
pontile, nodal and cranial nuclei would involve a discussion of the 
cranial nerves. 

Thus far I have attempted to give a brief resume of the modern 
views upon the sensory motor functions of the brain, and in doing so 
I have incidentally pointed out the localization symptoms of focal dis- 
ease within the encephalic mass. The localization of the mind and the 
relationship of these sensory motor functions to mentalization is a vastly 
more difficult problem. Nevertheless 1 will briefly attempt to indicate 
the probable direction which its future solution will take. 

Luys long ago remarked that certain convolutions were distended 
and hypertrophied when certain mental symptoms were present. In 
cases of delirium with delusions and hallucinations he found a pro- 
nounced gibbosity of the paracentral lobule to which a strictly motor 
function is usually assigned. Clinical observation has so far shown 
that only the motor zone possesses epileptogenous characteristics, 
though with epilepsy there are associated many sensory phenomena. It 
is unfortunate that in Lilys' observations no mention was made as to 
whether the delusions and hallucinations partook of the motor rather 
than of the sensory type; that is, whether they were mental representa- 
tions of abnormal kinesis or aesthesis. They seemed to show, at all 
events, that the cortical areas, both motor and sensory, are ideational 
and psychic, psychomotor and psycho-sensory rather than simply or- 
ganic. Mickle showed that hallucinations were due mostly to lesions 
in the sensory centers of the brain. 

The cells of the sensory areas an- preeminently receptive, and 
neither physiological experiment nor clinico-pathological observation 
has yet proved that they are in any wa\ emissive, except so far as they 
may send inhibitory impulses into the motor and into other sensory 
centers whereby there may be such a thing as a tactile paral) 
sensory aphasia. There can be little doubt that these sensory cells 






74 2 THE NON-NEURONIC DISEASES 

connected, mediately or immediately, with the motor cells of the cortex. 
These two sets of cells, thus intimately associated, form the summit, or 
bend, as it were, of the arc about which travel certain sensory motor 
impulses, and in all likelihood constitute the true physical basis of 
mind. Von Monakow declared at the Thirteenth International Medical 
Congress, held in 1900, that he believed that the diverse elements which 
had to do with the psychical functions were scattered all over the entire 
cerebral cortex. The gross character of the general sensibility and 
movements of the body, as compared with the special senses, necessi- 
tates a larger and grosser development of the centers that subserve the 
former functions than those that subserve the latter. This may be the 
reason, too, why they are more readily determined than the latter. In 
connection with sight and hearing, however, there is pretty conclusive 
proof that the sensory and motor cells are in close juxtaposition or at 
least functional association. It is a warrantable inference therefore 
that the same ideational centers cap, as it were, the arcs about which 
play the afferent and efferent impulses from the eye and ear. Hence I 
take it that the cerebral cortex is, after all, only a grand reflex center, 
the summit of the highest reflex arc. It is far more delicately organ- 
ized, more richly endowed with elements, and more keenly specialized 
than the reflex centers of the cord, but in all other respects it is quite 
comparable to the latter, both functionally and structurally. 

Midway between the sensory and motor elements and in countless 
interconnections with them are, of course, countless neurones and path- 
ways, commissural and associational tracts. Mind rests upon the whole 
basis, afferent, interpolated, and efferent tracts and centers. It is a 
product of their activity and not a -thing with a local habitat in this 
particular spot or ganglionic mass. This does not deny the possible 
existence of a metaphysical mind, but physiological and physiological 
psychology is incapable of taking up that question. 

The morphological and embryological development of the brain 
throws a flood of light upon the relations existing between the motor 
and sensory elements. Among the invertebrates there is, strictly speak- 
ing, no such brain or spinal cord as we find among the higher order of 
animals. Nevertheless, the spinal cord of the latter is clearly fore- 
shadowed in the series of sensory-motor ganglia with their respective 
projecting nerves found in the individual segments of the invertebrate. 
We know that in the articulates and insects each segment is furnished, 
as it were, with a little brain of its own, which is nothing more nor less 
than the summit of the reflex arc for that particular segment. We 
furthermore know that the ganglia of the more forward segments of 
the creature are but a hyperdevelopment, caused by an increase of local 
function, of that part of the primitive cord or elementary chain of 
ganglia. The explanation of the cranial nerves is only possible upon a 
Study of them from the evolutional and embryological standpoint; for 
whereas the visceral components of some of them, as. for instance, 
trie vagus, are still traceable to their primitive segmental origin, others 
have disappeared or become incorporated with adjoining sensory and 
motor nerves as to quite obscure their primitive simple arrangement. 
In the lower cord the visceral components of the segmental nerve stip- 



THE NON-NEURONIC DISEASES 743 

ply have completely disappeared or been replaced by the sympathetic, 
leaving only the cutaneous and muscular nerve supply represented in 
the posterior and anterior roots. All of which proves the primitive 
segmental structure of the entire cerebro-spinal axis. In some of the 
higher representatives of the worms and insects the ganglia of the 
most anterior part of the body become massed together and undergo a 
somewhat fuller development to subserve the purpose and function of 
special senses. In this way they assume in a measure the general char- 
acteristics of the vertebrate brain, and in their further phylogenetic de- 
velopment become so complex and changed in form and location as to 
involve their corresponding nerves in the same confused and complicat- 
ed condition. Hence the absence of that simplicity among the cranial 
nerves that we see in the arrangement of the spinal nerves. 

Note the exquisite arrangement — exquisite for simplicity — of the 
nervous S3 r stem of the white ant (Termes), of the fly (Musca), and of 
the scorpion spider (Thelyphonus caudatus). In all of these creatures 
the various segmental ganglia are connected with each other like the 
cells of an electric battery. Some of them are so far advanced in de- 
velopment that they simulate, without representing, the brain and spinal 
cord of the highest order of animals. In the vertebrates and even in 
their highest representatives, man and the apes, the primitive inverte- 
brate structure of the whole cerebro-spinal axis is not wholly lost. As 
Owen says, a vertebrate is a clothed sum of segments, and therefore 
is nothing but a higher invertebrate. In the lowest vertebrate, the 
amphioxus, there is only a spinal cord without, comparatively speaking, 
any brain ; and in all of its habits this humble creature closely resem- 
bles the invertebrates. Whether it be finally accepted or not that the 
human skull is composed of a number of metamorphosed vertebrae, the 
emibryological development of the brain and spinal cord out of the one 
continuous germ layer and the remarkable similarity of the brain and 
cord in their more gross structure and functions, are all extremely 
indicative of the primitive characteristics of the encephalon of man. 
If there be any truth whatever in the principle of evolution, it seems 
to me that it is not irrational to look upon the brain of the highest 
vertebrates as a more highly developed portion of the spinal marrow or 
ganglia of the cord lying most frontad. 

Tn speaking of what he calls the neurone-complex in its relation to 
brain function, von Monakow says that it is the sum of individual 
neurones, which articulate one from the other, forming progressively 
coordinate systems (projection systems of Meynert), of which systems 
the neurones become greater and greater in extenl as they approach the 
cortex (cells of projection and association) the minimum of winch is 
necessary to produce in the adult a simple nervous act such as a lumin- 
ous impression. Romanes, in his Mental Evolution in Animals, adopts 
a somewhat similar view when he undertakes an explanation of con- 
sciousness and its dej>endence upon the integrity of the cerebral e rtex ; 
for he likens cortical activity to the reflex function of the lower parts 
of the central nervous system, and then says thai consciousness is the 
result of the increased resistance which the original sensory impulses 
meet with in their passage through the more highly developed complex 






744 THE NON-NEURONIC DISEASES 

and intricate structure of the cortex. As von Monakow notes, the 
sensory tracts, upon which consciousness and intellection primarily de- 
pend, are composed of a great number of these "neurone-complexes," 
all of a similar nature, the more central of which are myelinized first, 
while the more peripheral ones are myelinized later. 

If all this be so, we should expect some similarity between the 
arrangement of the sensory-motor elements of the brain and those of 
the vertebral segments of the cord. The motor cells would not be 
identical with, but might lie in close proximity and intimate relationship 
with the corresponding sensory cells. The extreme simplicity of the 
arrangement of the cells in the cord is, of course, quite obliterated in 
the brain by the overcrowding of so vast a number of nervous elements 
in so confined a space as the cranium. The rolling about of the en- 
cephalic ganglia in their embryological and evolutional development, so 
as to accommodate themselves to the constrained limits of the skull, 
results in a more or less complete disappearance of that relative and 
simple arrangement of the sensory and motor elements seen in the 
vertebral segments of the cord. We can clearly recognize, however, 
that the ganglia and cerebral cortex are like the centers of the sensory 
motor reflex arcs found in the cornua of the cord. It is observable, for 
instance, in the relative arrangement and mutual development and de- 
pendence of the motor and sensory areas of the brain. General sensa- 
tion is the least specialized of man's sensory functions, and being co- 
extensive with the entire surface of the body, proves man's connection 
with the lower animals. The contemporaneous development, the simi- 
larity in extent and the relative anteroposterior location of the cortical 
sensory and motor areas, all reveal their connection with similarly re- 
lated parts of the body and their homology with the sensory-motor arcs 
of the cord. Their unusual development in size and functional activity 
gives them a preponderance over the corresponding segmental elements 
of the cord, and in their function, especially, makes them to appear as 
though they were voluntary while the latter are involuntary. But vol- 
untary and involuntary are relative terms, merely expressing different 
degrees of the same form of nervous activity. The psychic functions of 
the cerebral cortex are involuntary quite as much, if not in so glaring a 
manner, as are the involuntary functions of the various segments of 
the cord. They are both alike a form of reflex action, but instead of the 
cerebral reflexes being direct and unconscious, as the spinal reflexes are, 
the more sensitively and highly organized character of the cortex causes 
them to assume the nature of consciousness and self-will, while the con- 
nection of the cortex with the segments of the cord, as these in turn are 
again connected with one another, causes the cortical reflexes to be 
transmitted and perceived through the medium of the spinal centers 
rather than directly from the periphery of the body. In regard to the 
special senses of sight and hearing, the reflex sensory-motor arc does 
net pass through the cord or its ganglia, but is limited solely to the 
encephalic ganglia, while their sensory elements are always posterior 
to and more or less in close proximity with the motor elements just 
as they are in the spinal segments. 

The bilaterality of the cord, both in structure and in function, is 



THE NON-NEURONIC DISEASES 745 

duplicated in that of the encephalon. At the session of the Societe de 
biologie de Paris, May 25, 1889, M. Dupuy reported a case that showed 
the identity of the two hemispheres of the brain in regard to function. 
The patient possessed the power of moving the two eyes in different 
directions simultaneously. Even the perceptive centers seemed to be 
distinct, in spite of the opinion of Horsley to the contrary, for the 
young woman saw objects with one eye, and when she tried to use both 
eyes together to view the same object she was overcome with dizziness. 
Magnan has had four cases of this sort, one of which he reported in 
full. The patient heard one class of statements in one ear and another 
in the opposite ear. Agreeable ideas only were readily received on one 
side of the head, disagreeable ones on the other. The independence 
of the hemispheres has for a long time been a subject of discussion and 
partial acceptance among neurologists. Dr. C. L. Bruce reported in 
Brain, 1895, a case of double consciousness in regard to which he con- 
cluded that there was right hemispheric melancholia or dementia, with 
left hemispheric mania. Kiernan has also reported two cases which led 
him to believe in the independent action of the hemispheres. The com- 
ing possibility of a complete independence of action on the part of the 
hemispheres in regard to their higher, or psychic, function would 
seem to be foreshadowed in the fact already well recognized that the 
more complex and independent movements of the body, such as those 
of the hand, have less of a bilateral representation in the cortex than 
do those movements which are less complex, such as the movements 
of the respiratory and deglutitory muscles. Speech and its mechanism 
have attained such an exalted degree of development and specialization 
that they are already subserved by one hemisphere independently of the 
other. Phelps' recent conclusions from a large clinico-pathological 
analysis, that the left brain is the preeminent seat of the mental faculties, 
is indicative of the independence, in part at least, of the hemispheres. 
Brown-Sequard insisted long ago upon the identity of function in the 
two hemispheres, and physiold'gists are now beginning to recognize the 
truth of this fact and to admit the possibility of their independence of 
action. The whole question is most interestingly discussed by Dr. 
Ireland in his work The Blot on tJie Brain. 

I conclude, therefore, that man's mental activity is largely auto- 
matic and purely reflex; that the cortical centers for ideation arc con- 
stituted, localized and interrelated much like the reflex centers of the 
cord, but that the larger and more complex development of the former 
confers upon them the possibility of a higher and mon- complex form 
of activity; that the sensory and motor elements of the cortex are not 
identical, but are separate, are closely intermingled, and are most 
intimately associated with one another in function; and, finally, that 
mentalization is somehow subserved by the entire cortex and its more or 
less independence of action in the two hemispheres. 

If this progressive differentiation of function, based upon the 
principle of simple reflex action, continues within the encephalon as it 
has up to the present time in the evolutional development of the whole 
nervous system in animals, it may ultimately happen that the mind will 
acquire the power of thinking upon two or more subjects at one and 






746 THE NON-NEURONIC DISEASES 

the same moment. Its capabilities in this direction will be immensely 
enhanced, and the old dictum of the psychologists that the association 
of two or more ideas is always consecutive, never coincident, will be 
overthrown. In his essay upon the Molecular Dynamics of the En- 
cephalon, published in the American Journal of Insanity for October, 
1889, Dr. Williams hints at this future possibility. "Who knows," he 
asks, "but that the more fully evolved mind of the future shall learn, 
after the present mind has come to look with stunned discouragement 
upon the vast field of knowledge presented to its view by an advanced 
civilization, gradually to so adjust its fibres and its vessels by isolating 
them into separate fields momentarily (since the isolation is the acme 
aimed at by the higher mind in its concentrated workings to-day), that 
consciousness may, in fact, come to be not a single energy, but a double, 
triple, quadruple or multiple energy ? Imagine, for example, the school 
boy of the thirtieth century studying his mathematics visually with 
concentration, while orally listening to a lecture on a different topic. 
In all seriousness, there seem to be some reasons for believing that such 
a seemingly paradoxical mentality may be evolved." The tendency of 
mental and brain development is certainly in this direction. It is 
already so striking a characteristic of the human mind as to place man 
in a position above the lower animals. The separation of the various 
representative areas of the cortex, so that even now an animal can 
feel a prick of a pin in the foot, move the paw and listen intently to 
some unwonted sound, all at the same instant, would seem to give 
promise of such a future possibility in brain development. 

A mere glance at the localization of the various centers of the 
cerebro- spinal apparatus suggests the similarity of the brain and cord 
in regard to their primitive structure and inclines one to believe in 
the more ancient and higher development, both anatomically and physi- 
ologically, of the more forward part of this apparatus. The principle 
of inhibition, ever since its discovery in connection with the cardiac 
nerves, has been applied to the highe% cerebral functions, but with 
variable success until quite recently. When closely studied it appears 
that inhibition is the highest function of nervous matter. To inhibit an 
action and thus to control it, presupposes on the part of a nervous cen- 
ter a finer degree of organization than does the power merely to receive 
and transmit reflex impulses. Inhibition is the basal phenomenon of 
the higher mind, and is of such a startling character that it gives us 
the notion of an absolute independence resulting in free will. An 
afferent impulse is reflected into the motorial sphere, but is checked or 
inhibited by some other afferent impulse or impulses before it eventu- 
ates into actual movement ; and at once we jump to the conclusion that 
our free and independent will has been the cause of the motor phenom- 
ena. The inhibitory function of the mind is admitted by all the physi- 
ologists and psychologists. The former assert that were it not for 
this magnificent function of all the cerebral centers, or at least of some 
of the highest among them, our bodies would be kept in a constant 
state of convulsion through the manifold impulses which our nervous 
systems are ever receiving and reflecting outward again to the muscles. 
Mills speaks of the higher psychical centers in the forebrain as con- 



THE NON-NEUROXIC DISEASES 747 

stituting the "inhibiting lobe." When we recollect that all mentalization 
is based upon sensory and motor phenomena, and that the cortical 
areas for the psychical representation of these phenomena are quite 
fairly outlined, we are not surprised that there should be so much 
mystery surrounding the functions of the unknown areas of the brain. 
We noted that injuries of the prefrontal lobes always gave rise to 
mental deterioration with abnormal psychical phenomena, while the 
best physiologists admit that one function of this terra incognita of the 
cerebral cortex is at least that of inhibition. Putting all facts and in- 
ferences together, then, we may conclude that the power of inhibition is 
the last of the acquired functions and is in all probability the special 
characteristic of the most highly organized nervous matter; that this 
power resides in the gray matter of the prefrontal lobes to a very large 
degree ; and that therefore these lobes are preeminently the psychical 
centers, though the mind in toto is the result of the combined activities 
of all the sensory motor elements of the cortex. We may even infer that 
this anterior, highly specialized portion of the brain differs from the 
rest of the nervous apparatus in degree rather than in kind. 

Not only do the higher cerebral centers exercise an inhibitory con- 
trol over the spinal cord and lower centers, but certain cerebral centers 
clearly exercise the same function in relation to other cerebral centers. 
I suggested this fact a long time ago. This intracerebral inhibition was 
again pointed out by Pick, of Prague, before the Thirteenth Interna- 
tional Medical Congress in 1900, and illustrated by the inhibitory con- 
trol which the auditory speech centers exercise over the motor speech 
center. As is well known, persons suddenly attacked with word- 
deafness exhibit in addition to paraphasia, a special symptom, log- 
orrhcea. The importance of this in this connection is that it furnishes 
the first positive proof that in the sphere of the higher psychical phe- 
nomena, the mechanism of inhibition enters just the same as it docs 
in the domain of the lower nervous system. 

The known sensory and motor cerebral centers which have been 
described include, it will be remembered, the central convolutions, part 
of the first and second temporal, part of the occipital, the hippocampus. 
the uncus, and part of the limbic lobes. These areas are in connection 
with what Flechsig calls the projection system of fibres. In function 
they are identified with voluntary movement, general and tactile sense. 
bearing, sight, smell and taste. They represent approximately about 
One-third of the whole brain surface. The remaining two-thirds do not 
seem to connect with parts of the nervous apparatus lying below the 
brain, but with one another and with the parts already referred to. 
Flechsig calls these latter areas the "higher centers." or "association 
centers," and believes that they have to do especially with the com- 
plex mental acts, a view, however, in which he is not well supported by 
other authorities. As Sachs argues, projection and association fibres 
probably arise from every cortical area. Even Flechsig himself has 
recently admitted that the projection and association areas are not 
distinctly defined as he originally believed them to be. The generally 
accepted idea that the frontal lobes preside over the higher psychic 
phenomena need not preclude the idea that the entire C rt*tex is more 



74-8 THE NON-NEURONIC DISEASES 

or less involved in the act of thinking. As Hitzig remarks, Flechsig's 
opinions upon the purely intellectual function of the association areas 
are at the present moment extremely hypothetical. Even the theory 
which localizes the so-called memory-pictures in certain cell groups 
is not absolutely proved. About all that can be affirmed positively, as 
the result of the brilliant myelinization method of investigation em- 
ployed by Flechsig, is that in the cortex certain areas are primordial, 
in which areas the projection bundles are so much thicker than they 
are in other cortical territories ; and that the development of the sensory 
centers precedes in all likelihood that of the cortical areas which serve 
as a basis for the intellect. To go further than this and declare that 
the intellect is the result of special, limited cortical foci, with a par- 
ticular anatomical structure, as Flechsig is inclined to do, is hardly 
allowable. The work of Flechsig is admitted by all, however, to mark 
an important advance in our knowledge of the structure and function 
of the brain. 

In the evolution of the nervous system the centers of the medulla 
oblongata which preside over the vital processes may be the oldest in 
time. They are first because they are necessary to life itself. They 
take precedence phylogenetically. Ontogenetically, however, there are 
centers which precede even these in importance, and if, as the biologists 
tell us, the more highly organized matter is probably the more ancient 
(though this is not an established fact by any means), these higher 
psychical centers may be, after all, the oldest in time, while those of 
the medulla may be later differentiations of primitive nervous matter 
for the special regulation of the vital processes. It is not improbable, 
therefore, that the highly specialized inhibitory centers of the brain 
are the most ancient portions of the nervous apparatus, so far as their 
mere evolution is concerned, though from the embryological and physi- 
ological standpoint the cord is to be regarded as the primitive factor. 

In its influence upon the next lower centers the forebrain may be 
compared to the entire brain itself in its influence upon the centers of 
the medulla and spinal cord. In both cases the influence is chiefly 
inhibitory. Thus the inhibitory function is graduated from that of 
the highest psychical centers down to that of the lowest organic cen- 
ters of the cord where it is practically so overpowered by the supreme 
inhibitory influence of the highest centers, that it appears to be almost 
entirely absent, reducing the cord, as it were, to a mere organ of gross 
and unobstructed reflex action. From its evolution, therefore, the con- 
clusion may be drawn that the entire cerebro-spinal axis is a series of 
connected sensory motor ganglia, reflex couplets, or arcs, differing in 
its several parts more in degree than in kind. The more frontal ganglia 
subserve the purpose of psychosis, which in its highest manifestation 
is the expression of an inhibition and which differs from the spinal cord 
neurosis chiefly in respect to consciousness. Consciousness and its 
physiological explanation are in need of much elucidation ; its localiza- 
tion is still an undetermined question. Brain and spinal cord are never- 
theless shown to be mere arbitrary divisions of a uniform, continuous, 
composite organ whose functions are more or less the same throughout 



THE NON-NEURONIC DISEASES 749 

■all of its parts, these functions being simply adaptive modifications of 
the primitive sensory-motor reflex. 

SYMPTOMS OF DISEASE OF THE BRAIX. 

The nervous system, as I have previously pointed out, is a uni- 
form, similarly arranged network of neurones throughout all of its 
parts. Every evidence points to the fact that these neurones possess, 
per se, the same general functions wherever they may be located. In- 
tracranial neurones are no different, structurally or functionally, from 
intraspinal neurones. Association and commissural tracts are prac- 
tically the same as projection tracts and their extension into peripheral 
nerves. The only dissimilarity between different parts of this vast and 
beautiful network of irritable cells called neurones is to be found in 
certain adventitious elements, such as the sustentacular structures and 
the end-organs. 

The nervous system is a single organ with a single uniform func- 
tion. Neural irritability and self-nutrition are its only essential func- 
tions when it is contemplated apart from all of its mere connections 
with other organs and its juxtaposition to certain connective-tissue and 
vascular elements. If it were thus entirely independent and separate 
from everything else, its symptomatology would be a matter of mar- 
velous simplicity. 

The simple function of neurility, or nervous irritability, inherent in 
the neurones, is, however, made to appear very complex and varied by 
the fact that different groups of neurones are connected with different 
structures in different parts of the body. So far as the neurones them- 
selves are concerned, sensation is the same in the optic as it is in the 
spinal neurones ; motion is the same in the facial nerve neurones as it 
is in the cardiac nerve neurones ; secretion is the same in the salivary 
gland neurones as it is in the renal cell neurones. To the particular 
end-organs of sense, motion and secretion, the neurones merely fur- 
nish a peculiar form of irritability ; or, to state it better, they are irri- 
tated in their own peculiar way by certain sensory organs, which irrita- 
tion they transfer, as a form of excitability, over to certain motor and 
secretory organs. The functions of the nervous apparatus may thus 
be regarded as primary and secondary. Neurility and self-nutrition arc 
its primary functions; motion, sensation, trophism are its secondary 
functions. 

In the diagnosis of a nervous disease the pathological diagnosis 
involves, and is largely dependent upon, the disturbances of the primary 
functions. Primary and secondary degenerations, inflammations, etc., 
all have to do with the manifestation of neurility and self-nutrition in 
the nervous elements. We have no special names for these primary 
Symptomatic manifestations of disease in the neurones, because at the 
time that neurological nomenclature was created the neuronic structure 
of the nervous apparatus was unknown. We use the terms paralysis, 
irritation, spasm sometimes in the sense of deficient or exaggerated 
neurone irritability. It is obvious, though, that tin- utius are used in 
a metaphorical sense. We are applying, in using them, our ideas 






750 THE N0N-NEUR0NIC DISEASES 

formed from muscular manifestations to the neurone manifestations^ 
We say a nerve is paralyzed, whereas the word paralysis specifically 
means loss of motion or sensation. This loss of motion or sensation 
may indeed be due to the death of the neurones, but it may also be 
due to damage in the muscular tissue or sensory end-organ. It is ob- 
vious that we are in need of a nomenclature to distinguish neurone ces- 
sation of function apart from mere muscular or sensory cessation of 
function. Until we have such a nomenclature, we must still go on 
applying terms symptomatic of non-neural disturbances to the symp- 
tomatic exhibitions of pure neural disturbances. Because of this hiatus 
in neurological nomenclature, it is all the more imperative that we 
should most carefully distinguish the neural from the non-neural mani- 
iestations of disease. We must be careful not to attribute every 
paralysis to nervous trouble. We must not imagine that every visual 
disturbance is indicative of disease in the eyeball. We must not fancy 
that every parsesthesia is a sign of neuronic disorder. Like a great wall 
around the nervous system is the aggregate of all these peripheral end- 
organs that are in relation to it. Behind this wall is hiding the nervous 
network which is uniform in structure and function throughout all of 
its parts. There are diseases which belong to and damage the end- 
organs or outer wall. There are diseases that damage the nervous ap- 
paratus hiding behind it. The two must be carefully differentiated, else 
most disastrous blunders will be made. 

Nine-tenths of neurological diagnostic criteria involve the mani- 
festations in the outer wall around the nervous apparatus, the end- 
organs. As these end-organs are so varied, we have a varied symp- 
tomatology. In this way we localize lesions within the nervous system. 
I repeat with emphasis that these localization symptoms which are 
based upon the secondary functions of the nervous apparatus must not 
be imagined as giving us any special information as to the primary or 
neuronic disturbances. Inferentially they help us to determine whether 
the disease is neural or non-neural, but only inferentially. The latter 
must be made out from the etiology and certain special phenomena like 
the electrical reaction of degeneration. 

The localization symptoms being the most obtrusive, and those 
upon which we must largely depend in the making of our diagnosis, 
it is profitable that we should discuss them along general lines before 
taking them up in detail under the head of special diseases. 

The ideal localization of neurological manifestations would, of 
course, be the neuronic. We have attained this desirable goal in re- 
gard to a few diseases. We recognize the neuronic localization of the 
lesion, for instance, in locomotor ataxia, progressive muscular atrophy, 
certain degenerative neuritides. In time we may determine the neuronic 
localization of many more, if not all, of the special diseases to which 
the nervous apparatus is liable. We may be able in time to localize the 
neurones that are at fault in hysterical and other psychic troubles. At 
present our knowledge of nervous physiology is so small and coarse 
that in many of our localizations we cannot get farther than such crude 
anatomical subdivisions as the brain, spinal cord and nerves. We have 
refined a little upon these crude localizations without yet attaining to 



THE NON-NEURONIC DISEASES 75 1 

the neuronic refinement of them. Thus, in the brain we have discov- 
ered certain areas of the cortex as having certain peripheral relation- 
ships that give them apparently distinct, secondary functions. The 
outlines of these areas, however, are still most obscure and their inter- 
relationships with one another are still mysterious. In regard to other 
parts of the cortex and the great central ganglia at the base of the 
brain, we know practically nothing, though functionally they are at the 
basis of mentalization and other cerebral phenomena. 

In a coarse way, then, we can distinguish what we are pleased to 
call brain symptoms. A few of these brain symptoms have been dis- 
cussed in the previous section upon the Physiology of the Brain and 
Cerebral Localization. Here I purpose to recapitulate a few of the 
more important manifestations which indicate in a rough way disease 01 
that part of the nervous apparatus that happens to constitute the cere- 
brum. The symptoms of disease of the medulla and cerebellum will be 
considered later. 

In the making of a diagnosis it is important, first, to decide that 
the trouble is a brain disease, and secondly, to localize the lesion in some 
part of the brain. The former can be decided from general symptoms ; 
the latter must be made from focal symptoms. 

General Symptoms of Disease of the Braix. — Of these head- 
ache is probably one of the most common. Nearly every disease of the 
brain, whether neuronic or non-neuronic, organic or functional, is more 
or less accompanied by headache. It must not be inferred from this, 
however, that all headaches point to brain disease. There are many 
nerves in and about the head that may be variously affected without the 
brain being the direct source of the pain. Nevertheless, it is a most 
important truth that when the brain is affected, headache is sometime 
or other present. 

It would lead me too far to discuss cerebral headaches here; es- 
pecially as I have taken up the subject of cephalalgia in a special 
chapter. 

By itself, headache is of very little value as a symptom. In con- 
junction with other symptoms it is of tHe greatest value. In organic 
cerebral disease the headache is somewhat definitely localized, is asso- 
ciated with tenderness upon percussion, is more or less constant, though 
it may be with periods of exacerbation, and is of a dull, boring char- 
acter, or sharp, knife-like and penetrating. It is increased by such 
sensory irritation as loud noises, bright light, sudden jars caused bv 
coughing, sneezing, etc. Circulatory disturbances may modify it. In 
the psychoneuroses, such as hysteria and neurasthenia, it is apt to be 
more diffuse, variable as to intensity and location, and to a certain 
extent under the influence of the mind. 

Vomiting of a particular type is characteristic of brain disease. 
It is spoken of as cerebral or nervous vomiting. The suddenness of 
it has caused it to be named "projectile" vomiting. It is frequently 
associated with headache, and comes and disappears with the nervous 
exacerbations. It is usually not dependent upon the ingestion of food, 
but may take place at most unexpected times. It is devoid of Strain. 
In all these respects it is unlike the vomiting of gastric disorder. The 



752 THE NON-NEURONIC DISEASES 

vomiting of alcoholism is a gastric symptom. The vomiting of fever, 
unemia, migraine, hysteria and some cases of neurasthenia is due to 
cerebral disturbance. The most characteristic form of projectile emesis 
is seen in tumor of the cerebellum and medulla. In combination with 
other symptoms it is all but pathognomonic of disease here. It occurs 
in meningitis, abscess, hemorrhage and other lesions that increase the 
intracranial pressure. Irritation of the gastric vagus center in the 
medulla is the probable explanation of it. 

Nausea may or may not accompany the vomiting. Sometimes it is 
very distressing. Occasionally it occurs without the hyperemesis. 
Vomiting, with or without nausea, associated with cephalalgia and not 
accountable for on the ground of gastric trouble, should arouse the 
strongest sort of a suspicion of intracranial disease. An immediate 
examination of the eyes is then called for to' determine the absence or 
presence of choked disc. 

Vertigo is not an important brain symptom. It is not the same 
as incoordination or mere loss of equilibrium, which is so marked a 
feature in cerebellar disease. As I have discussed the nature of vertigo 
in considerable detail in a section by itself, I will omit further consid- 
eration of it here. 

Temperature. — Elevation of the temperature accompanies many 
affections of the brain, but it is due to the general disease process and 
not to the special fact that the latter is located in the brain. Infectious 
inflammatory states produce fever when they attack the brain, just the 
same as when they attack any other organ. It is not always easy to 
determine how much of the temperature is due to the general infection 
and how much to the local inflammation constituting part of that 
general infection. A tubercular meningitis may exhibit an elevated 
temperature, not on account of the inflamed meninges so much as on 
account of the general constitutional tuberculosis. 

Sometimes there is a rise of temperature in disease of the brain 
when the pathological process is not markedly inflammatory. It is then 
the expression of a disturbed nervous function. Very high tempera- 
tures occur thus. Lesions of the pons and medulla, especially, provoke 
such pure neurotic temperatures. They may even run as high as 10S 
degrees F. and be very misleading. In hysteria, neurasthenia and other 
neuroses, neurotic elevation of temperature certainly does occur at 
times. There are supposed to be heat regulating centers in the brain, 
and they probably are intimately associated with the vasomotor centers. 
It is a difficult matter at times to differentiate a mere nervous elevation 
of temperature from one due to an infectious or inflammatory process. 
It may be said, however, that pure nervous temperatures are apt to 
be sudden, changeable and temporary. The pulse does not exhibit any 
corresponding relationship to them. When they are very high they 
are usually bad signs. 

Sometimes there is a serious intracranial disease without any 
alteration of the temperature. 

In the initial stage of cerebral hemorrhage the temperature drops 
below the normal. 

Pulse. — It is a curious fact that the pulse may be much less fre- 



THE NON-NEURONIC DISEASES 753 

quent in febrile disease of the brain than it would be with the same 
febrile affection in any other organ. In some diseases of the brain it 
may be subnormal. This is seen in tumor and abscess. Simple inflam- 
matory and infectious processes usually have a rapid pulse, though 
there is less frequently here than in disease elsewhere a correspondence 
between the pulse and the temperature. A rapid pulse may indicate 
damage to the vagus center in the medulla. The slow pulse of menin- 
gitis in children, of apoplexy and of general intracranial pressure is 
believed to be due to over-action of the inhibitory .center upon the heart. 

Respiration. — The respiratory phenomena of brain disease are 
numerous and important. The respirations are usually diminished 
when the brain functions are lowered. I recently saw a dangerous ex- 
ample of this in a case of chronic lead encephalopathy. In coma and 
stupor it is often lessened. In meningitis and apoplectic strokes it 
assumes the Cheyne-Stokes type and becomes a bad omen. This type 
of breathing occurs in other diseases, such as pneumonia, scarlet fever, 
diphtheria, opium poisoning, but it is a less grave symptom in them 
than it is in brain disease. 

In the Cheyne-Stokes breathing there is a remarkable cycle of 
increasing and decreasing depth. There are first a few superficial 
breaths. These gradually increase in rapidity and depth and become 
noisy. Then a fall takes place until there is actual cessation. After 
a pause, however, the slight respiratory movements begin again, grad- 
itally increase in intensity, until there is a deep dyspnceal breathing 
once more and the respirations again lessen. The pupils usually con- 
tract and the heart action diminishes during the pause, which may 
last from five to forty seconds. The duration of the cycle may be 
fifteen to seventy-five seconds. Never do the respirations of each 
cycle exceed thirty in number. 

Sometimes the respirations begin with great suddenness. Some- 
times they begin and terminate suddenly. This has been seen in 
meningitis and is known as Biot's type of breathing. 

Irregular breathing and cessation of breathing occur in disease of 
ihe medulla. Under such circumstances the heart has been seen to 
continue in action and death was prevented by artificial respiration. 

Renal symptoms may be indicative of disease of the brain, but 
more often they are concomitant manifestations. Albuminuria and 
glycosuria, more frequently polyuria, accompany lesions in the medul- 
la. Cardiac disease and renal trouble are not infrequently associated 
with cerebral vascular disorders. Mental disorders are the caua 
urinary and faecal incontinence when there is no paralysis of the vesical 
and rectal sphincters. The polyuria of the neuroses and psychoneur 
such as hysteria and certain spasmodic troubles, need only to be men- 
tioned. 

Psychic Symptoms. Psychosis. — The symptoms which I have 
considered up to this point are so general in character that they only 
point to intracranial disease when they are associated with other more 
suggestive signs. Many of them occur in other diseases. They are 
therefore not in the least distinctively encephalic. 

The symptoms which we are now about to take up point to the 



754 THE NON-NEURONIC DISEASES 

brain, but while often dependent directly upon brain disease, they are 
not necessarily so in all cases. 

A psychosis means a mental aberration, an unusual exhibition of 
mental manifestation. Were we acquainted with the true nature of the 
mind, there would be less confusion in connection with these symp- 
toms and their localizing worth would be greater than it is. 

The seat of the mind is assumed to be the brain ; some say the 
anterior part of the frontal lobe. It has even been affirmed that in 
right-handed people it is in the anterior left frontal lobe. As a matter 
of fact, we know nothing of its localization. It probably has its chief 
focus of manifestation in the brain cortex, because there the highest 
neurone cell-bodies are located, but that its existence is not due solely to 
the cortex in its healthy state is shown by the fact that it can be made 
to exhibit most extraordinary and even insane manifestations by dis- 
ease in parts of the body remote from the brain. In other words, mind 
is more or less coextensive with the nervous mechanism. 

How are we to explain this apparent contradiction that the mind 
is located in the brain and yet is so subject to remote neural disorders? 
It seems to me that no psychology offers so clear an explanation as 
does the voluntaristic psychology so. ably taught by Wundt, of Ger- 
many. 

The mind is not a thing or entity with a local seat. It is but the 
name which we apply to the internal interplay of the afferent impulses 
one upon the other. It is a pure function, a secondary product. Even 
the use of the term product is misleading, for mind is not even pro- 
duced from something; it is the something itself, and that something 
is the inner operation of the thousand and one impulses passing up to 
the brain along the afferent pathways and playing against and in and 
out among themselves. They are the same impulses, perhaps slightly 
modified in the cord, that started from the periphery, but now in their 
aggregate complex intermingling constitute what we call the mind. 
Mental activity is but the insi'de view of the neurone activities whose 
outside view is given us by physiology. 

Physiology is the objective contemplation of elementary nervous 
functions ; psychology is their subjective contemplation. 

Physiology and psychology are thus facing each other and are 
explaining from directly opposite points of view the same set of neural 
manifestations. They both analyze and combine the phenomena which 
present themselves in the workings of the nervous system on the 
outward and the inward sides respectively. Outwardly the physio- 
logical elements are the neurones and their manifestations under vari- 
ous stimuli. Inwardly the psychological elements are the sensations 
and feelings. When the outer elements are collected together and 
work normally, we have a normal, physiological nervous apparatus; 
when the inner elements are taken in the aggregate and work together 
normally, we have the normal manifestation of mind. The psychic 
elements include the five senses and the feelings associated with them. 
Out of the innumerable combinations and recombinations of these 
psychic elements the various faculties of the mind, such as the mem- 






THE NON-NEURONIC DISEASES 755 

on', the imagination, the will, the judgment, are evolved. To show 
how would be, of course, beyond the province of this work. 

This physiological psychology and explanation of mind is called 
voluntaristic because it teaches that all of the faculties, like the volition, 
are mere processes. It has long been recognized that volition is but a 
convenient term to express the overflow of certain afferent impulses into 
efferent impulses. The will is not something apart by itself ; it is a 
high order of functional manifestation between certain psychic ele- 
ments ; which psychic elements in turn are but the inner representation 
of the primary physiological sensations. What is true of the will is 
true of the mind and all of its so-called faculties, and hence the name 
voluntaristic for this psychology. 

I felt it necessary to introduce here this brief statement of the 
voluntaristic explanation of mind, because it underlies the explanations 
of the psychoses presented in this work. 

The mind being thus seen to be dependent upon the physical senses, 
just as a chord struck upon the piano is dependent upon the individual 
notes, but not being the same as the physical senses, but rather the 
result of their aggregate activities, just as the musical chord is not the 
same as the individual notes, but is something different resulting from 
their aggregate sound, it can readily be understood how it can be 
disarranged by disturbance both in the individual senses and in their 
mere interrelation to each other. Just as an inharmonious chord can 
be produced out of a harmonious chord upon the pianoforte by one 
note of the chord being broken on the one hand or by the introduction, 
abstraction or other disarrangement among the notes themselves ; so a 
psychosis can be set up by a physical disease in any one or more of the 
anatomico-physiological elements upon which mind depends, or by a 
functional disarrangement among the elements which otherwise may be 
perfectly norma). In this way we can account for mental symptoms 
that sometimes seem to be due to actual physical disease and that at 
other times do not seem to have any apparent physical basis at all. 
For example, maniacal manifestations are sometimes clearly due to 
gross meningo-encephalitic changes ; at other times, as in certain forms 
<»f insanity, they seem to occur without any discoverable physical basis. 
Hysterical exhibitions are clearly enough due to physical diseases in 
some instances; in other instances no changes of a physical sort have 
ever been detected. In the former case the psychosis was a physical 
phenomenon ; in the latter it was purely a functional exhibition. 

The reader will now understand why the psychic symptoms which 
I am about to tabulate are not absolutely indicative of organic brain 
disease, though they are always indicative of the functional disturbance 
of the mind. He will also note how important it is not to jump to an 
immediate conclusion that the brain Is diseased or tin- mind hopelessly 
affected as soon as any of the following mental symptoms show them- 
selves. The cause of these symptoms must always be sought for first 
in some physical disease. If this is removed, they may vanish, [n 
some cases, however, these mental symptoms will appear without the 
existence of any physical disease. They are probably the result then 
of disarranged action among the primary psychic elements, such as is 



75^ THE NON'-NEURONIC DISEASES 

sometimes seen in the primary psychoses like the primary hysterias and 
fundamental insanities. None but psychic treatment can hope to reach 
these cases, and even that cannot be expected to do much in severe 
examples. 

Wundt has shown that there are two sets of psychic elements, the 
psychic sensations and the feelings, out of which the entire mind is 
elaborated. The sensations are the psychic counterparts of the physio- 
logical five senses. They combine and interplay to form the memory, 
imagination, reason, judgment and intellectual faculties. The feelings 
are the indefinable appreciation of the psychical sensations ; they are 
accompaniments of the latter. They are the result of the functional 
appreciation of the psychic elements by the combined product of those 
elements, or the beginning mind or ego. The}' are the counterparts, 
therefore, in a way, of the objectively combined physiological elements 
that enter into the constitution of a normal nervous mechanism. They 
combine to form emotions, which emotions determine the motives, and 
so on up to the elaboration of the will. At the bottom of mind are the 
psychic sensations and psychic feelings ; at the top, and gradually 
elaborated out of these along two lines, as it were, are the judgment and 
the volition. 

When the mind is affected with disease the top, of course, falls 
and the amount of the loss is proportional to the extent of the disease. 
The judgment and the will are the first to topple. The next lower 
processes are thus left without the inhibition normally exercised upon 
them by the higher faculties. In this way we see in disease the imag- 
ination on the one hand running riot in all sorts of delusions, and the 
emotions on the other hand bursting out into uncontrollable exaltations 
and depressions. If still more of the mind is overthrown, the imagina- 
tion and the emotions disappear, amnesia is present and the victim 
sits in a condition of stupor. The next stage still lower is one of 
complete dementia, with the patient in a mere vegetative state. The 
last stage is the total abolition of all mind or mental death. This last 
condition is probably never seen so long as the lower or vegetative 
functions are active, for even the lowest idiot has a trace of a con- 
scious mind still left. Total abolition of mind is only present in death. 
As a temporary condition, total abolition is seen in coma of a profound 
type. 

I will now trace downward this gradual disappearance of the mind 
as it is seen in the more common psychic manifestations of brain 
disease. 

Abnormal Intellectual States. — These, of course, are innumerable 
and varied, but as they are the outgrowth of psychic sensations, they 
involve illusions, hallucinations and delusions. The basal elements be- 
ing disturbed, the composite ideas and all their inter-connections in the 
most exalted forms of mental acts are also disturbed. Hence conscious- 
ness, attention, cognition and recognition, memory, imagination and 
reasoning are all more or less upset. 

An Musi oil is a misinterpretation of an external impression. By 
reason of disorder in the transmitting apparatus, afferent special and 
common sensory nerves and their endings, an impulse is perceived dif- 



THE XON-NEURONTC DISEASES 757 

ferently from what it should be. The essential feature of an illusion is 
that there is an actual external stimulation of the nerves, but it is not 
recognized in its true light. Illusions may occur through any of the 
avenues of sense, but they are most common in the visual and auditory 
fields. The victim of illusions beholds a brother, say, and mistakes him 
for a total stranger ; he hears a whistle and declares a cat mewed ; he 
lifts a feather and it seems like a piece of lead. 

Mild, temporary illusions are common enough in ordinary life 
among perfectly normal people. Our senses are not perfect and they 
are constantly giving us inaccurate information; but we immediately 
correct the errors and so go on as normal beings about our occupations. 
The insane individual is not able to correct his illusions and so he 
acts accordingly in a way that is most extraordinary and unusual. 

The immediate cause of many illusions can readily be discovered 
in the afferent peripheral apparatus. It may be wax in the ear that is 
disturbing the ingoing auditory impulses. A stone in the bladder 
may be interpreted by the patient's sensorium as a small animal that 
has gotten in there. Most of the so-called hallucinations in childhood 
are really illusions. Pavor nocturnus may sometimes be due to them. 

In the majority of cases the immediate cause of illusions is a dis- 
order in the perceptive center. This is shown by the fact that the 
illusions often harmonize with the delusions present and thus partake 
somewhat of the nature of hallucinations. It is obvious that an illu- 
sion does not necessarily represent a very profound degree of mental 
alienation. It becomes a sign of insanity only when it remains un- 
corrected. 

A deeper degree of mental disturbance is revealed in a hallu- 
cination. Here non-existent objects and impressions are perceived; 
or, in other words, the sensorium projects into the outer world, through 
the avenues of sense, its own formed sensations, which sensations are 
the result of a disorder in the sense-apparatus or nerve-center. 

Unlike illusions, hallucinations are more than mere misinterpreta- 
tions of veritable stimuli. They are the perception of stimuli that are 
immediate to the sensorium, but are accepted as being veritably objec- 
tive and outside of the sense-apparatus. 

Hallucinations are also common in normal life, but not so com- 
mon as illusions. They are immediately corrected in the same way as 
the latter. The continuous feeling of the absent member in an ampu- 
tated arm or leg is an excellent illustration of an hallucination. Kvery 
one has heard a noise sometime or other when there was actual silence, 
or seen the shadow of a figure when no person was near. Illusions and 
hallucinations play a large role in spiritualistic phenomena and the 
seances elaborately built up upon them. Hallucinations arc due to a 
disorder of the sensory nerve centers and are therefore more serious and 
fundamental than are illusions, which are usually due to disease in the 
peripheral sensory apparatus. 

Hallucinations often partake of the nature of the patient's de- 
lusions and thus represent a most advanced state of alienation. Mis 
delusions being of a persecutory character, say, he assumes a frightened 
manner, begs to be protected and shows in every way that he imagines 






75& THE NON-NEURONIC DISEASES 

he sees those who are going to harm him. Some of the attitudes of 
hystero-epilepsy are undoubtedly due to these delusion hallucinations. 
They occur in some sane people under high excitement and when they 
are between sleep and waking. Baillarger calls these psychic hallu- 
cinations, or pseudo-hallucinations. 

Hallucinations may be due to irritations in the cortex, but they are 
not regarded as signs of insanity so long as the subject of them is 
able to correct them and recognize their nature. Hallucinations under- 
lie many of the assaults and murders committed by the insane. 

Delusions are false beliefs. Illusions and hallucinations represent 
primary disorder in the psychic elements and therefore in the psychic 
ideas which are the outgrowth of these elements. When the inter-con- 
nections especially between these psychical ideas or compounds are 
disordered, delusions make their appearance. Delusions are therefore 
generally indicative of a most profound sort of mental aberration, be- 
cause they are not immediately dependent upon disorder in anatomico- 
physiological elements, but in the functional interplay and inter-con- 
nection between the psychical elements and compounds which are de- 
pendent upon them. Delusions are radical and decidedly mental. They 
may be dependent upon a physical disease in a physical basis, but they 
are also, and usually, dependent upon a complicated and complex func- 
tional disturbance in a very high order of mechanism. 

Delusions may occur in health as well as disease. It is difficult to 
draw a sharp line between the delusions of sanity and insanity. Estab- 
lished beliefs and convictions must be taken into account. The whole 
history of mankind is full of false beliefs. If these are not corrected 
by later knowledge, those who continue to live under them are not 
considered insane. If they are corrected, then those who still retain 
them are regarded as mentally unbalanced. Believers in astrology, 
witchcraft and mythological gods are deemed mentally diseased if they 
live in the heart of modern civilization. They would not have been 
deemed so had they lived in earlier times or did they now live among 
barbarians. Therefore the ability of the victim to correct his delusions 
must be considered when the latter are being considered as signs of 
mental alienation. Because we cannot always determine that ability, 
from our want of knowledge in regard to the patient's early influences, 
education and present environment, it is sometimes a difficult question 
to decide as to whether his delusions are insane or merely eccentric. 
The laity have a ready rule for determining what they consider de- 
lusions; for they hold everybody crazy that do not hold the beliefs 
that they do. To the scientific physician, however, falls the arduous 
task to compare the delusions with all that makes up the patient's past 
history and his present environment, and from that comparison deduce 
his conclusions as to their sane or insane origin. It is the province of 
psychiatry to lay down the guiding principles whereby the physician 
is to arrive at a final opinion. 

Delusions may be sensorial or ideal. The former arc founded upon 
illusions and hallucinations. If these are persistent and uncorrected, 
and the patient acts in accordance with them, he is said to be deluded. 
His entire mentalization is under the control of the illusion or hallu- 






THE NON-NEURONIC DISEASES 759 

cination. Ideal delusions are spontaneous false concepts, unrelated to 
any sensory disturbances. A patient who believes that he is a million- 
aire, that he has a thousand children, that he is one of the twelve 
apostles, is the victim of an ideal delusion. These delusions are prom- 
inent in the religious sphere because religion, or man's dependence 
upon a superior, protecting Intelligence, is an ancient and primitive 
concept. They may occur in any sphere, however, especially the sexual, 
alimentary and in the higher regions of thought. 

Many of the obsessions of the psychoneuroses, the imperative con- 
ceptions, the fixed ideas, the phobias mentioned under the head of neu- 
rasthenia, are of the nature of ideal delusions. The difficulty in eradi- 
cating them sometimes is recognized by every clinician and shows the 
profound depth of their origin. At other times, fortunately, they are 
so slight as to be scarcely more than the similar delusions held by per- 
sons in perfect health. 

Delusions occur in toxic conditions (lead, cannabis indica, alcohol, 
etc.), in low adynamic states, in starvation and in the delirium of acute 
general diseases. 

Abnormal Emotional States. — As I have pointed out, the emo- 
tional states are the outgrowth of those psychic elements called the 
feelings. The feelings are the accompaniments of the psychic sensa- 
tions. Whereas the latter lead up to the intellect, the feelings by com- 
bination and recombination ultimately lead up to the will. There are 
mental disturbances that show themselves prominently in the emo- 
tional sphere, just as there are others that exhibit themselves promi- 
nently in the intellectual sphere. In most diseases both spheres are 
more or less implicated together. 

The abnormal emotional states assume the character of exaltations 
and depressions. These range all the way from health up to actual 
maniacal excitation of the most violent sort, or down to a most extra- 
ordinary depth of melancholic stupor or pure indifference. 

In normal individuals we often observe a high degree of emotion- 
ality. Emotions underlie the motives, as the word itself indicates — 
e-motives. These e-motives combine and overflow into the motor sphere 
and we have the manifestation of volition. If they are weak and inade- 
quate, there is no volition and the subject remains inactive. 

Exaltation and depression are usually dependent upon the relative 
activity of the mental processes. In exaltation, as its name indicates, 
there is excess of ideation, of muscular power (apparently?), of circula- 
tion, of visceral activity and of the appetites. These reactions are 
stimulating and pleasurable. Hence exaltation is usually accompanied 
by an ecstatic, satisfied and happy frame of mind. This, however, may 
easily run over into incoherence, verbal delirium, muscular excitability 
and physical violence. The condition is seen in mania, mania sine 
delirio, dementia paralytica, etc. 

This exaltation may be due to nervous weakness (loss of inhibi- 
tion), as well as to excess of nervous force. It may alternate with 
states of depression. 

Exaltation is sometimes termed psy clamp sia because, like muscular 
spasm, it is a sort of mental over-action or psychic spasm. 



760 THE NON-NEURON IC DISEASES 

Depression is usually accompanied by corresponding physical con- 
ditions. There is general debility, lowered muscular power, sluggish 
visceral functions, reduced appetites, retarded metamorphosis. It is the 
opposite of stimulation and therefore not pleasurable. For this reason 
it is often termed psychalgia, or psychic pain. There is a w r ant of voli- 
tion here, a want of speech, a want of interest. Usually there is intense 
melancholy. This may pass over into complete stupor and indifference. 
An appearance of indifference must not mislead the physician, however, 
into thinking that it is real always. In many cases there is psychic 
hyperesthesia, but it is so keen and so painful psychically that all other 
psychic manifestations are completely paralyzed and an attitude of 
utter, profound indifference is assumed. Depression is seen in melan- 
cholia, in hysteria, in neurasthenia and in the prodromal stage of mania 
and dementia paralytica. 

The consciousness is often disturbed and its disturbance is among 
some of the most important of the brain symptoms. Upon the basis 
of the voluntaristic psychology, consciousness is the name for the gen- 
eral synthesis of psychical processes, in which general synthesis the 
single compounds are marked off as more intimate combinations. When 
this inter-connection of compounds (ideas and emotions) is interrupted, 
there is deep sleep, a faint, or coma. 

Disturbances of consciousness involve abnormal changes in the 
combination of psychical compounds, even though the compounds them- 
selves show no internal changes whatever. This is a most important 
distinction, for upon it we can explain many of the phenomena of dis- 
ease which involve the conscious state as apart from the mere intellec- 
tual and emotional states referred to above. There are probably in- 
numerable forms of disturbed consciousness, but we recognize in prac- 
tical semeiology only a few, and these I will now refer to briefly. 

Delirium is a characteristic disturbance of consciousness in which 
there is mental confusion and excitement with hallucinations, motor 
restlessness and illogical and incoherent thinking expressed in words 
and acts that betray the condition present. The mental processes are 
here perverted. The delirium may be active or quiet, low and mutter- 
ing or wild and exhausting. It is not so common a manifestation of 
organic brain disease as it is of cerebral intoxication, infection and 
fever. In the delirium grave, or Bell's mania, the symptom is most 
typically observed. There are alternations of active, loquacious periods, 
with violent struggling and attempts to leap out of the window, etc. 
I have often noticed that the hallucinations revolved around some line 
of thought which deeply concerned the patient before the disease ap- 
peared. Hallucinations of speech and act, indicating a basis of fear, 
may thus have some slight foundation. Often, however, there is no 
accounting for the direction of the hallucinations. They seem to spring 
up utterly without rhyme or reason. 

Loss of Consciousness. — Here there is a complete suppression of 
the mind. The psychic elements themselves have been abolished, or 
their interplay has been completely annulled. This condition is close 
to sleep. In fact, it is a comoulsory sleep with certain attendant phe- 
nomena. It is a very common symptom of brain disease. It occurs 



THE NON-NEURONIC DISEASES 761 

under many varied conditions. It may be partial or complete. The 
mere vegetative functions of the body, the heart action and respiration, 
need not necessarily be affected in coma, though often they are. 
Hebetude, stupor, somnolence, sopor and coma are all degrees of the 
loss of consciousness. Stimulation can arouse the patient less and less 
as he passes from the first into the last. In coma the sensations, the 
reflexes and all avenues to the mind seem to be absolutely closed. The 
whole brain is usually affected in these conditions. 

Tumor, abscess, tuberculous meningitis and other forms of intra- 
cranial pressure and intoxication frequently are accompanied by mental 
stupor and dullness. The patient is listless and indifferent, but can 
be aroused into a momentary exhibition of intelligence. He seems to 
be resting under a cloud, which again closes over his mind as soon as 
he is left to himself. In somnolence the stupor assumes a deeper shade 
and resembles profound slumber. In these states the urine and faeces 
are often involuntarily passed, though the sphincters are normal. Food 
placed in the mouth may at first be chewed and then is left there with- 
out further mastication. The patient seems to have suddenly gone to 
sleep in the very midst of the act. In coma there is no response what- 
ever and there is no attempt at chewing and swallowing unless the 
coma is very light. 

The loss of consciousness may come on gradually or abruptly. It 
is not the same as syncope exactly, and yet in both phenomena the 
immediate cause is the anaemia of the cortex. Symptomatically the 
great feature of coma is the loss of all sensibility. It is seen in epileptic 
seizures, in surgical cerebral compression or concussion, in uraemic 
poisoning, in acute alcoholism, in toxic narcosis from opiates, morphia, 
chloral, etc., and in congestive or malignant malarial fever. Its most 
typical manifestation is probably observed in cerebral apoplexy, whether 
hemorrhagic or embolic. 

The differential diagnosis of the different forms of coma will be 
found under the heads of the disease in which it occurs. However, it 
is so important a symptom that a brief recapitulation will not be out 
of order here. 

In epileptic coma one must look for signs of a previous attack, 
such as the lacerated tongue, the ecchymoses on the face, neck and 
chest, the frothy saliva, the involuntary micturition or seminal dis- 
charge. The coma is of brief duration and i.s followed by a small rise 
of temperature. 

The unconsciousness of cerebral concussion or compression is asso- 
ciated with injury about the head or body, oozing from tin- cars or 
nose of blood, meningeal hemorrhage with gradual stupor without 
pronounced hemiplegia. 

In urcemic coma there is anasarca and slow pulse. If the urine is 
drawn by catheter and tested, it is albuminous and contains casts. The 
ophthalmoscope reveals a ncuro-rctinitis. 

In alcoholic coma the patient can be aroused, it is more of a 
condition of stupor. The breath is alcoholic and the temperature may 
be normal or subnormal. Alcohol can sometimes be found in the 
urine. 



762 THE N0N-NEUR0N1C DISEASES 

In malignant malarial coma there are no physical or paralytic 
symptoms, though the rectal temperature is high. The spleen is en- 
larged. The blood examination for the plasmodium is final. 

Opium narcosis is characterized by contracted pupils, subnormal 
temperature and slow respiration. 

Apoplectic coma is profoundly paralytic. There is hemiplegia 
with conjugate deviation of the head and eyes, the patient looking to- 
wards the lesion. The pupils are dilated. The temperature, at first sub- 
normal, soon rises. 

The Cheyne-Stokes respiration, pupillary changes, alterations in 
volume and rate of the pulse beat are all accompaniments, though not 
important ones, of the comatose state. 

Double consciousness is a condition of the mind seen in certain 
hysterical states, such as the hypnotic and somnambulic, and in certain 
forms of epilepsy and insanity. The patient seems to have both a 
normal and a morbid mind and she alternates from one to the other. 
Some remarkable cases of this trouble have been seen. It is purely a 
mental disorder and seems to be due to a partial abeyance at times of 
the mind. It occurs in a slight form in hysterics and sometimes it is 
the cause of the strange wanderings and doings of epileptics. 

Amnesia. Mental Failure. — Loss of memory is a common sign of 
brain disease. It occurs in the mildest neuroses. It may be so marked 
that the condition becomes one of actual dementia. Retention is the 
first requisite of all mental activity. None of the higher faculties can 
exist if memory is gone. Chronic and disseminated diseases of the 
cortex usually have among their earliest and prominent symptoms 
amnesia. There are special types of amnesia, which, however, are not 
of sufficient importance to need detailed description here. 

There are certain psycho-sensory and psycho -motor states that 
might very appropriately be discussed here under the head of the 
psychic manifestations of brain disease. They are, for instance, word- 
deafness, word-blindness or alexia, and the disorders of speech included 
under the name of aphasia. As I have pointed out under the head of 
Cerebral Localizations, there are areas in the cortex that in some 
mysterious way subserve the performance of these complicated acts, 
such as speech and writing. For clinical purposes we can use these 
acts as localizing signs, and for that reason I will discuss theni along 
with the other more distinctive focal signs of brain disease in the fol- 
lowing sections. 

I desire here, however, to emphasize the fact that speech, reading, 
word-hearing and writing are psycho-physical exhibitions, and to pro- 
test against the too common assumption that they are the result of 
certain physical activities in certain limited groups of cells called 
"cortical centers." A speech-center, a writing-center may indeed rep- 
resent the point of convergence or physical inter-connection for all 
those anatomico-physiological processes that underlie the correspond- 
ing psycho-physical manifestations. Ablation of these centers neces- 
sarily breaks up the psychic phenomena dependent upon them and ex- 
pressed physically through them, but that these centers are special 
independent little organs, as it were, for the performance of the func- 



THE NON-NEUBONIC DISEASES 763 

tion of speech, of reading, of writing, etc., none but the crudest tyro 
in psychological investigation would for a moment believe. Regarding 
this point, which I have long insisted upon, I can do no better than 
quote a paragraph from Wundt : "When the destruction of certain 
cortical regions produces definite disturbances, in voluntary move- 
ments and sensations, or when such a destruction interferes with the 
formation of certain classes of ideas, it is perfectly justifiable to con- 
clude that these regions furnish certain indispensable links in the chain 
of physical processes which run parallel to the psychical processes in 
question. The assumptions often made on the basis of these phenom- 
ena, that there is in the brain a special organ for the faculties of speech 
and writing, or that visual, tonal and verbal ideas are stored in special 
cortical cells, are not only the results of the grossest physiological mis- 
conceptions, but they are irreconcilable with the psychological analysis 
of these functions. Psychologically regarded, these asumptions are 
nothing but modern revivals of that most unfortunate form of faculty- 
psychology known as phrenology." 

DISTURBANCES OF LANGUAGE. 

Most authors treat of these symptoms under the general name of 
speech disturbances. I prefer the use of the word language, because 
it has a broader meaning than the word speech has come to possess in 
popular parlance. I believe that much confusion has been thrown 
around this entire subject by the difficulty one has in thinking of speech 
in the bread sense that we think of language. Speech has come to be 
rather synonymous with emissive language and more particularly 
articulated emissive language. It is not easy to think of written speech 
or mere pantomimic speech, and it is next to impossible to regard un- 
worded speech, whether receptive, inherent or emissive in relation to 
the brain, in the same clear, well-defined light that we regard verbal or 
articulated speech. The word language, it seems to me, is so broad and 
yet so accurate that it can well replace the confusing word speech. 

Language is the power of communicating ideas to another. It 
makes no difference in what manner or by what agencies the communi- 
cation is made, whether with vocal sounds, with recorded symbols, 
with gesture movements, it is all language. A mere touch of the hand 
may convey an idea to a receptive subject: a simple wink may mean 
yes or no as much as the spoken or written word. Nay, more, it is not 
even necessary that the person to whom the ideas are being communi- 
cated should understand either the spoken, written or gestured sign. 
So long as a sign of some sort stands for the ideas in the mind of him 
who is trying to communicate them, it constitutes a language. A 
Hottentot may try ever so hard to communicate his ideas to me. He 
has a language, even though I comprehend not an iota of his vocal 
utterances, his graphic signs or his gesture movements. He has his 
ideas, that is obvious; and he has his own particular symbols for them, 
which he has adopted for himself. Those symbols constitute hi> lan- 
guage. By means of them he attempts to communicate his ideas 
another individual, whether that individual be a human or an animal. 



764 THE N0N-NEURON1C DISEASES 

Indeed, he communicates the ideas to himself by them, or, in other 
words, he attaches to those ideas of his own certain adventitious, fixed 
symbols which even to himself he uses to fix and recall the ideas nec- 
essary for the continuance of his thinking. 

In its last analysis, then, language is nothing more or less than 
the symbolising of ideas. This is a most important fact to grasp before 
beginning the discussion of the disturbances of language. 

In the definition of language two things must be clearly empha- 
sized. The first is that it is a symbol, a sign, a something in place of 
something else. The symbolizing is not conferred upon living creatures 
from without, but it springs originally from within. A symbol is first 
formed in the mind ; is first employed there ; and is then expressed 
outwardly. In this way language begins in animals and infants. Mere 
sounds, for instance, like mama or papa, originally without meaning 
and uttered by the infant in its feeble struggles to make its little ideas 
known to those about it, have become crystallized into words. Origin- 
ally, however, they were nothing but sounds and meant, as symbols of 
ideas, nothing more or less than the crow of the cock or the call of 
the moose. 

The so-called roots of civilized speech when traced back to their 
source reveal the fact that primitive language was imitative as far as 
possible. The savage who rubs two sticks together to convey an idea 
to his fellow savage is employing a language as much as the dog who 
barks and leads his master to the drowning child, or as that child when. 
it cries and stretches out its hands to the nursing bottle. . 

All of these movements and noises are for the purpose of com- 
municating ideas. In time these movements and noises, by repetition, 
by the unconscious process of mutual agreement, by combination and 
recombination, become the fixed symbols of higher language. They 
first represent something in the mind of the animal to his own mind,, 
and thus they become the basis of his thinking. The capacity to form 
and retain these symbols is what distinguishes man as a higher think- 
ing animal than the brute. Babies cannot think like adults and one 
adult cannot think like another adult, largely because their powers of 
fixing these linguistic symbols within their psychic mechanism is weak. 

Language, therefore, as an aggregate of symbols springs out of 
thinking and in turn assists the processes of thought. I hope the reader 
has noted that in the evolution of language it is thought that gives it 
birth. If animals had no thoughts, however primitive they may be,, 
language would never come into existence. 

This leads to the second point that should be emphasized in the 
definition of language — namely, that it is for the communication or 
representation of ideas. If ideas are wanting, there will be no lan- 
guage. Now animals make sounds and perform acts that are not based 
upon any ideas, such, for instance, as the thousand and one reflex acts, 
the acts of mere vegetative life, that never become language and in 
themselves are not in the least linguistic. They only become linguistic 
the moment they are made to take the place of an idea, the moment they 
are adopted as symbols for a thought. Winking, for instance, is per- 



THE NON-NEURONIC DISEASES 765 

formed as a mere reflex act a thousand times a day ; it is not language 
until it is made to suggest some idea. 

The essential point in language then is that it is a symbol for 
ideas. As I have said before, it is perfectly inconsequential as to what 
the character of the symbol may be, whether it is known to any other 
than to the one who adopts it, so long as it is a symbol and so long as it 
stands for an idea, it is language. 

This is not the place to go into further detail in regard to this 
fascinating subject, the development of language, but I felt that the 
above brief notice of it was necessary to emphasize the fact, which seems 
to be lost sight of by some physiologists in their discussion of the 
cortical speech centers, that language is a psychic and not a mere 
physiological phenomenon. It is the outward panorama, as it were, of 
ideas. Every discussion of it and its disturbance involves a discussion 
of the nature of ideas. These, as I have shown elsewhere, are what 
we call in modern physiological psychology, psychical compounds. 
They represent combinations between psychical sensations and the feel- 
ings. The psychical sensations and feelings are the correlates of and 
riave as their parallel physiological bases, the five senses of the body. 
Ideas being thus shown to be complex and compound processes, it must 
follow that language based upon them must have a compound and 
complex structure. It is therefore useless to look for specific centers 
in the brain for the elaboration of psychic manifestations, which in their 
very nature show that they are compounded of many psycho-physical 
processes. Physiologists are awakening to the fact that speech centers, 
such as they used to be thought of, do not exist in the brain. There are 
groups of cells here and there in the cortex that undoubtedly subserve 
the purpose of bringing together widely divergent processes and so far 
as these groups of cells subserve the function of symbolizing ideas they 
may be spoken of as speech or language centers. These so-called speech 
centers are available for localizing purposes. Their connections with 
other centers are in a few instances so well known that we can ofttimes 
localize a lesion very definitely when the intervening association tracts 
are damaged. Under no circumstances, however, are we justified in 
attributing the function of speech to any one cortical area or subcortical 
tract. 

Only by clearly recognizing the above described nature of language 
and its relation to all of the cortical, and perhaps subcortical, functions 
can we explain some of the strange phenomena observed in focal 
lesions which we had expected from our physiology to produce a defi- 
nite set of linguistic symptoms. To account for some of these unex- 
pected manifestations, those who ignore psychology entirely and believe 
that the evidences of physiology point to special cortical spots as the 
source of such complicated psycho-physiological phenomena as speak- 
ing, reading, writing are, have to resort to some very queer and illog- 
ical reasoning. Thus they talk about individual variations . contradict- 
ing, as it were, their own position when they found their physiologica] 
teachings upon such narrow, materialistic bases a- they doj They say 
one person uses his visual memory more than another in his speech; 
another his auditory; a third his motor. .Ml of this is true and in 



766 THE NON-NEURONIC DISEASES 

itself reveals that language is a compound, variable process, a func- 
tional psychosis, and not, as they have just been stating, a physiological 
manifestation in certain fixed parts of the cortex. In one sentence they 
show that mind is not an entity, that psychosis is not a thing, but a' 
function, a process, an interplay between certain lower and more 
elementary psycho-physiological sensations ; and yet in the next sen- 
tence they try to fix that mere function, process or interplay in the 
anatomico-physiological functions of a few nerve cells and fibres 
grouped in so-called centers. No wonder they say with a half-surprised 
manner, "the loss of a certain center will cause a hardly noticeable dis- 
order in one and a severe and persistent disturbance in another." - 
Elaborate paradigms are constructed based upon the idea that speech 
is subserved by special cortical centers, and yet immediately after the 
paradigms it is stated that partial lesions occur very often (a fact not 
always demonstrable, though too often assumed), and that such cases 
cannot be grouped in the paradigms. 

Disturbances of language, then, are psychic symptoms. They are 
not more definite as localization symptoms than are some of the illu- 
sions and hallucinations previously referred to. Their definiteness 
occurs on account of the sphere in which they occur — namely, the sym- 
bolizing of ideas. In the manufacture of these symbols, animals use 
movements and the secondary result of a particular form of movement, 
sound. Behind all language, therefore, is some form of motility. If 
this motility involves the sound producing apparatus, we have loss of 
' articulate speech. This may be purely paralytic. The muscles con- 
cerned may be directly paralyzed or immobile. This is a disturbance 
in articular speech. It is called anarthria if it is complete; dysarthria 
if it is incomplete. The muscles, with their nerve supply, that are 
involved are those of the lips, tongue, palate, larynx and respiratory 
apparatus. Sounds may be made if all of the muscles are not paralyzed, 
but they cannot be articulated into definite forms to subserve the pur- 
poses of speech. When sounds cannot be produced the condition is 
known as aphonia. A patient suffering from anarthria need not neces- 
sarily be aphonic. He can make a noise, but he can't speak, because 
some of his muscles refuse to work. 

The muscles by which speech is articulated are innervated from 
the nuclei of the medulla, hence their paralysis is usually a bulbar 
symptom. But these nuclei are under the control of the higher centers 
in the cortex. They may be paralyzed, therefore, from disease in these 
cortical centers, as, for instance, the facial and hypoglossal near the 
bottom of the central convolutions. As these cortical areas are repre- 
sented in the opposite hemisphere and the two sets are intimately con- 
nected by commissural tracts, cortical paralysis of the muscles of articu- 
lation is not apt to be permanent. Symmetrical disease in the hemi- 
spheres, however, may permanently damage the articulation. This is 
what is known as pseudobulbar paralysis, because it so closely simu- 
lates disease of the medulla. 

All degrees of paralysis may occur from disease of the bulb. 
The speech may be only slightly deranged, or it may be so profoundly 
affected that nothing but sounds are heard. When the lips are paral- 



THE NON-NEURONIC DISEASES 767 

yzed, p, b and m are sounded like f snd v ; when the tongue is affected, 
the 1 and t resemble y and th ; implication of the palate turns p and b, 
the explosive labials, into the continuous labial m, because the posterior 
nares cannot be shut off. 

Other slighter forms of dysarthria are the confluent and elisive, 
when the consonants and syllables are run together; and the staccato 
or scanning speech, when the syllables are unduly separated as one sep- 
arates them when he is scanning a line of poetry. These defects are 
all self-evident and their examination needs no special description. 

We have just seen that language, spoken as well as other forms of 
language, is something more than the utterance of noises, etc. It is a 
symbolic utterance of sound. The sound must be made in a particular 
way to convey the proper idea. This necessitates the employment of the 
muscles in a particular, combined manner. The manner must be 
thought out in the brain before it is put into execution. If the word 
to be uttered, the symbol, belongs to old and fixed language, the in- 
dividual's memory will be involved in his thinking as to how he should 
put the muscles of his vocal apparatus to produce just the sound he 
wants to. It is obvious that in this process, which after long years of 
practice has become subconscious in part, a fine, delicate coordinating 
mechanism is involved. The focus of this mechanism, or rather the 
foci of these mechanisms, constitute what are called the cortical speech 
centers. Disease of these centers causes a loss of language. This is 
known as aphasia. 

Aphasia, then, does not mean paralysis in the sense that anarthria 
does. It means merely psychic paralysis for language. It stands for a 
loss of the memory pictures of speech, the loss of the power of sym- 
bolizing one's ideas. As symbols are various, but always involving a 
motor idea, aphasia is of a varied type, but is always related to motility 
more or less. Complete aphasia would involve all forms of symboliza- 
tion and as a result would represent a condition in which there is no 
language whatever. That would probably mean a condition in which 
there were no ideas, or complete idiocy. Partial aphasia would mean 
that the power of symbolizing one's thoughts is lost in one way but 
not in another. 

Several forms of partial aphasia are now recognized clinically, 
though there are doubtless innumerable forms that are so fine as to 
quite escape ordinary detection. Those that are clinically recognized 
are motor or ataxic aphasia, amnesic aphasia, alexia and agraphia. 
Pantomimic or gesture aphasia and paraphasia should be included. 

These are all forms of language defect and represent a disorder 
in the psycho-sensory-motor mechanism that underlies the whole process 
of language production. There is, of course, a parallel physiological 
sensory motor mechanism in the cerebral cortex, certain of whose 
points we can recognize in the motor speech center of Broca, the 
sensory speech center of Wernicke and the centers for word-blindness, 
etc. Of these the first is the most definite, doubtless because the funda- 
mental purpose of language being the fixation and communication of 
ideas by symbols and symbolization being fundamentally a motor and 
emissive process, every form of speech has in it actually, or represented 



768 THE NON-NEURONIC DISEASES 

in it potentially, some form of motility. Even receptive speech and the 
unuttered language of thinking are essentially emissive for it is a process 
wherein the mind communicates to itself, as it were, in another form 
its own ideas. As t«he emissive process can only take place over the 
motor pathways, we have in every word, every form of language the 
motor element lurking. We have discovered that the anatomico-physi- 
ological concomitant of this motor manifestation resides in the group 
of cells known as Broca's center, and to some extent all of the motor 
centers. These are in communication with the hearing and visual and 
touch centers, wherein reside those cellular elements that associate 
sounds and sights with the muscular movements in such a way as con- 
stitutes the aggregate network out of which the linguistic function is 
evolved. 

The interconnections in this basal sensory motor network is the 
essential point to note, for it is upon them that what we call language 
has its foundations. The network may be broken here or there so that 
there is a partial rupture in the sensory motor complexus, or the group 
of cells that here and there serve to unite the various parts of the net 
may be obliterated. In this way we have the partial and the special 
types of aphasia established. That there are innumerable types of 
aphasia, indicating countless possible breaks in this wonderful com- 
plexus of sensory motor inter-connections more than we can now locate, 
is hinted at in such manifestations as the forgetting of particular names, 
of particular gestures and of particular forms of print. 

Language is the product of an associative process; not of mere 
cell activity per se. It is a psychic phenomenon resulting from inter- 
connections between sensory and motor elements. The so-called centers 
of language are merely the points at which some of these fundamental 
inter-connections are most obviously brought about. Aphasia is the 
result of a break somewhere in the network of inter-connections. If 
the break is at the so-called centers, the aphasia may be grossly and 
wholly motor or sensory in type. If the break is between the centers 
it may merely sever the motor from the sensory side of the complexus, 
or it may sever one form of motor from another form of motor element 
in it, or one sensory from another sensory element in it. As the inter- 
connections are fine and innumerable, so the ruptures may be fine and 
innumerable. 

I will now take up and discuss a few of the gross ruptures which 
we recognize chiefly. The reader will find some assistance possibly in 
the section devoted to the consideration of the Cerebral Localizations. 

Motor Aphasia. — The term ataxic as applied to this form of aphasia 
should be dropped, because ataxia can be produced by sensory as well 
as motor disturbances. Motor aphasia is usually produced by a lesion 
at the base of the third, left frontal convolution, Broca's center, in 
right-handed people. The corresponding area in the opposite hemi- 
sphere is the active one in left-handed individuals. Disease of one side 
is occasionally compensated for by development of the function of the 
other side, thus causing the aphasia, under certain conditions, to ulti- 
mately pass away. Disease anywhere in the conducting path from the 
center also produces motor aphasia. 



THE NON-NEURONIC DISEASES 769 

Motor aphasia is a loss of voluntary speech. There is a distinct 
want of memory pictures by which the muscular apparatus is put into 
condition to emit the desired sound. An aphasic patient is not speech- 
less. He can utter words and often automatically can roll off long- 
grammatical sentences. Verses that he has memorized can often be 
correctly recited. Singing, which usually automatically sustains rhe 
verses, often makes the task exceedingly easy. Even a commonplace 
automatic conversation can be carried on in mild cases. The moment, 
however, the conversation becomes voluntary and unusual, it halts and 
delays. Irrelevant words and sentences are introduced. Wrong words 
are used. Words having opposite meaning from those intended are 
uttered. Syllables are misplaced and doubled. 

Complete motor aphasia is practically always accompanied by right 
hemiplegia. Bastian saw the exceptional instance in which a left- 
handed person experienced a lesion of the left hemisphere and had 
right aphasia with right-sided hemiplegia. 

Sensory Aphasia, IVord-Dcafness. — Here the patient is in the con- 
dition of a person listening to an unknown foreign language. He 
hears the sounds correctly but they mean nothing to him. They are 
only sounds. There is no actual deafness. 

This form of aphasia often accompanies the motor. It is easily 
tested by asking the patient to do or say something. He stands mute. 
He has heard but he does not comprehend. Voluntary speech, if this 
amnesic type of aphasia only is present, is ready enough. Reading and 
writing, except from dictation, are carried on normally. Alexia and 
agraphia, however, are very often present. The extent and character 
of the lesion determine this. The seat of the disease is here located in 
the first, left temporal convolution in right-handed persons. The es- 
sential trouble is the loss of the memory pictures for sounded words. 

Some impairment of speech may be caused by this amnesic aphasia 
from its interference with the processes of thought. Thinking neces- 
sitates the use of symbols and in higher language-using animals, like 
man, the vocal symbols are made to serve the processes of ratiocina- 
tion. When the memory of these vocal symbols is gone it is obvious 
that the thinking processes are lowered and especially the utterance of 
those processes in words that must be searched for partly in the 
affected region. Mechanical or automatic speech is therefore better 
in amnesic aphasics than spontaneous, voluntary speech; and mere 
spontaneous, voluntary speech is easier than a conversation, in which 
the mind is not left so much to its own devices. This inability to 
awaken word tone pictures in one's self, apart from the mere loss of 
word-perception, is called amnestic aphasia. The higher psychic cen- 
ters are disconnected from the ordinary language centers, though audi- 
tory impulses reach and stimulate- the latter. 

Agraphia. — This may occur alone hut it more generally accom- 
panies motor aphasia. There is some doubt as to the nature of this 
symptom. It is clearly a motor or psycho-motor disturbance. Some 
have supposed it was due to disease in Broca's center, because as they 
say, internal motor vocal speech always precedes its outward expres- 
sion in writing. Motor agraphia, however, does occur apart from ordi- 



yyO THE NON-NEURONIC DISEASES 

nary motor aphasia. The trouble, moreover, seems to be more deeply- 
seated than would be a mere loss of memory pictures for movements 
in the right arm and hand, for the patients cannot even form the words 
out of lettered blocks placed before them. It probably represents a 
much larger disconnection in the linguistic network than is represented 
in any one center or single tract. No such special center is known to 
exist. If inner speech precedes written speech, there may be a discon- 
nection between Broca's center and that for the hand. Most frequently 
agraphia accompanies verbal sensory aphasia and motor aphasia. 

As I have shown, language is practically always an emissive sen- 
sory-motor phenomenon ; hence internal language must somewhat in- 
volve both sensory and motor processes before it is uttered in writing 
or any other way. These patients can very often write from printed 
copy though they cannot write from diction. They do not, of couse, 
understand or comprehend what they are copying. The visual appara- 
tus takes in the letters on the page and the hand reproduces them. The 
patient is like one who is copying an unfamiliar, foreign language. 

Alexia or Word-blindness. — This may be isolated, though it usu- 
ally accompanies sensory aphasia. A lesion has often been found in 
these cases in the angular gyrus in the left lower parietal lobe. Here 
the tracts course that connect the visual centers in the occipital lobe 
with the auditory center in the temporal lobe. The reason for the 
frequent association of alexia and amnesic aphasia is that an internal 
language must be presupposed before an intelligent comprehension 
of that which comes in by way of the visual apparatus can be expected. 
These patients with alexia are like persons reading an unknown, for- 
eign tongue. They see but they do not comprehend. Of course, writ- 
ing is impossible to them. This is not the agraphia just described, for 
spontaneous writing and writing from verbal dictation (in isolated 
alexia) is easy enough. The alexic patient cannot write because the 
graphic symbols are absolutely unintelligible to him. In agraphia the 
disturbance of the comprehension of language precedes and prevents 
the inditing of symbols ; in alexia the disturbance of the comprehension 
of language follows the writing instantaneously. The latter is like a 
man trying to build a brick wall, who, the moment he lays the brick 
down it ceases to be to him a brick or a wall, but something absolutely 
different and irrelevant. Curiously, such patients can sometimes read 
writing by tracing the outlines of the letter with their finger. The 
sensory pathways of the arm are here made the connecting link be- 
tween the written language and the intact speech centers. 

Pure alexia, as I have been describing, is of subcortical origin. 
Right hemianopsia for obvious anatomical reasons, often accompanies 
pure alexia. 

Visual Aphasia. — This is a rare condition in which objects are 
seen and recognized but cannot be called by name, though they can 
be named if in any way they can be perceived through the other senses. 
Let such a patient look at a bell, for instance, and he cannot name it ; 
let the bell be sounded, however, and he at once states what it is. 

Lesions in this curious condition have been discovered at the 
border of the left occipital and temporal lobes ; but they have always 



THE NON-NEURONIC DISEASES 771 

been extensive enough to implicate both tracts from the occipital* 
visual areas to the sensory speech center in the temporal lobe. Alexia., 
hemianopsia and sensory aphasia usual!}- accompany this condition. 
Oppenheim asserts that he finds this trouble not uncommon in otitic 
cerebral abscess. 

In tactile aphasia, which is exceedingly rare, objects that are 
touched cannot be named. This must not be confused with astereog- 
nosis. 

Xo discussion of aphasia is complete without a notice of the 
disorders of pantomime. These occur among aphasics and involve the 
gesture language. Amimia and paramimia have a similar import to 
aphasia and paraphasia. A pantomimic action is the product of a psy- 
chic process. It is therefore something more than a mere emphatic 
gesture. These patients nod "yes" when they mean "no." 

The causes of aphasia may be functional or organic. As I have 
shown elsewhere a pyschosis is the only nervous disease that can be 
strictly functional unless we include many forms of reflex disturb- 
ances under the name functional. It is possible to have a disorder in 
the interplay and interconnection between perfectly normal psycho- 
physical elements. Among the organic causes of aphasia are to be in- 
cluded the toxic causes that upset the basic neurones. 

It is only on the possibility of a psychosis being a true functional 
manifestation that we can explain the fact that aphasia may follow a 
severe fright and occur in hysteric states. In migraine it is probably 
associated with vasomotor disorder. It. of course, can be produced in 
a reflex way. It has thus been seen in children as the result of worms 
and minor surgical operations. 

Exhausted states of the blood and the nervous system may give 
rise to it. Among the toxic antecedents are to be recorded the acute 
infectious fevers, such as typhoid, pneumonia, scarlatina, nephritic con- 
ditions with uraemia, carcinoma, gout and in santonin poisoning. 

By far the most common organic cause is focal encephalomalacia 
because it is so frequently a cortical trouble. Softening is more fre- 
quently a cause than is hemorrhage. The middle cerebral artery, espe- 
cially the left, that is so frequently the seat of these vascular troubles, 
is the artery that supplies the most important language-production re- 
gion of the brain. As a rule lesions in the deeper parts, the central 
ganglia and internal capsule, do not cause aphasia. They maw how- 
ever, if they are large enough to compress the cortical areas. In uni- 
lateral lesions that do not compress these parts, the speech emissive- 
impulses find their way to the opposite hemisphere by way of the cor- 
pus callosum, and so on outward. 

Cerebral abscess may cause amnesic aphasia. Motor aphasia has 
followed abscesses also of traumatic and metastatic origin. 

Pressure aphasia may accompany suitably located intracranial neo- 
plasms. In children tuberculosis and tuberculous meningitis are some- 
times responsible. 

Gonorrheal embolism has been blamed for it by Tit res and limns. 
Direct traumatism is a factor in the etiology. A congenital aphasia has 
been observed. It is probably due to a prenatal or natal hemorrhage. 



772 THE NON-NEURONIC DISEASES 

Toxic and functional aphasia usually disappear soon and com- 
pletely. As an indirect focal symptom it may disappear if the original 
cause changes so as to relieve the pressure (hemorrhage) or obstruc- 
tion (embolism). Usually it requires several weeks or months, though 
a week or so may see it vanish. In children, there is always the pos- 
sibility of the right hemisphere taking up the function when the left 
is damaged beyond recovery. The nature of the cause and its amena- 
bility to treatment obviously determine the prognosis. 

The treatment, further spoken of under the head of cerebral hem- 
orrhage and softening, involves removal of the cause, combating the 
underlying disease, and re-educating the patient. A correct diagnosis 
as to the nature of the loss of speech and a little ingenuity in setting 
the linguistic tasks for the patient to practice daily is all that need to 
be suggested here. 

Motor Symptoms. — Irritative Symptoms. Convulsions. — These 
may be provoked by direct irritation, as in meningitis or tumor ; or by 
the alteration of the gray matter in regard to its nutrition. Irritations 
of the cortical motor zone, of course, affect the opposite side of the 
body, as all the cortico-spinal motor tracts decussate. As a result tonic 
and clonic spasms occur which may be limited to certain movements 
or involve all the movements. When the irritation is bilateral, the 
convulsion is general. In this way we have monospasms, hemispasms 
and universal convulsions. The movements may begin with twitchings 
or they may start in a tonic spasm and pass into the clonic state. Oft- 
times a twitching will begin in a certain small area and then spread 
gradually until a large part or even the whole body is convulsed. There 
is no fixed rule as to the succession of parts involved. Generally the 
progress of events can be seen in the spasms to be proceeding up or 
down the central convolutions. Thus if the movement starts in the 
leg, it attacks next the arm and finally the face ; or if the face is the 
earliest seat of the manifestation, it passes next to the arm and finally 
to the leg. A convulsion that starts in the arm is apt to involve the 
face before it does the leg. 

In monospasms, consciousness is not disturbed. When, however, 
the convulsion becomes general, consciousness is usually lost. 

These localized monospasms are spoken of as partial or cortical 
epilepsy. As manifestations of Jacksoniau epilepsy, I have discussed 
them elsewhere. It is a question whether all organic, gross, irritative 
lesions that provoke such monospasms should be regarded as epileptic. 
They are epileptiform. They occur in organic and functional troubles. 
Toxic conditions, such as alcoholism, uraemia, saturninism, seem to be 
capable of producing them, though it is not improbable that these are 
merely organic also, being due to hemorrhagic and embolic alterations 
of a minute character. 

A temporary paresis usually follows these manifestations. If it 
remains it means that the lesion is more than an irritative one. It has 
begun to exercise a destructive influence upon the affected cortical area. 

Sensation is often implicated with these irritative motor phenom- 
ena. There may be various paresthesia* in the limb that is subjected 
to the spasm. It may be only an accompanying symptom or it may be 



THE NON-NEURONIC DISEASES 7/3 

the sole symptom in the form of an equivalent. It is now believed 
that the sensory elements are most intimately intermingled with the 
motor, or at least are intimately interconnected, so that it may well be 
that the true irritative epilepsies in this case are really sensory phe- 
nomena with secondary motor manifestations, even as occurs in gen- 
eral epilepsy. Cortical epilepsy occurs from irritative subcortical 
lesions but disappears absolutely when the cortex is destroyed. 

Choreic and athetoid manifestations are irritative symptoms but 
they are not believed to be due to cortical irritation. As they usually 
occur in hemiplegic conditions they are thought to depend upon the 
irritation of the thalamus. They occur more frequently in disease of 
the thalamus and are best discussed after hemiplegia. 

A tetanoid spasm has been observed in disease of the cerebellum, 
or other lesion that produces increased pressure beneath the tentorium. 
The head is bent backward with opisthotonos, the jaws are clenched 
and the whole appearance is that of traumatic tetanus. Forced move- 
ments occur. It is not known whether the symptom is indicative of 
cerebellar or pontile disease. The condition lasts sometimes for hours, 
though the tonic contraction is broken by clonic jerkings. 

General convulsions, due to disease of the brain, such as tumor, 
embolic hemiplegia, and meningitis, may so closely simulate hysteria as 
to deserve the adjective hysteroid. 

Paralytic Symptoms. Monoplegia. Hemiplegia. — The first great 
characteristic of cerebral paralysis is that it is distinctly of the voli- 
tional power over the musculature. In diseases of the lower motor 
segment, the paralysis, of course, will have all the appearance of being 
in the volitional sphere, because this segment lies between the upper seg- 
ment and the musculature, and therefore cuts off impulses passing 
from one to the other. In the muscles, however, that are partly vol- 
untary and partly involuntary, as for instance, the muscles^of respira- 
tion and deglutition, it is rendered obvious enough when the volun- 
tary movements are impossible from upper segment disease, while the 
involuntary movements continue intact. 

A second great characteristic of brain palsy is that, for evident 
anatomical reasons, the muscles are not affected with a true atrophy. 
Their nutrition is dependent primarily upon the ganglionic cells in the 
anterior horns of the cord. For the same reason there is no reaction of 
degeneration observed in cerebral palsies. 

As the upper or cerebral motor segment exercises an inhibitory 
control over the lower, when it is diseased, the paralysis is accompanied 
by an increase of all the relieves. This i> a third important charac- 
teristic of cerebral paralysis. 

A fourth is that the paralysis affects the movements of the body 
rather than the mere individual muscles. The areas of the cerebral 
cortex subserve facial movements, arm movements, leg movements, 
etc. A cerebral paralysis never picks out special muscles, hut only 
those muscles and their antagonists thai normally arc employed in the 
production of higher, purposive psycho-motor activities. This type of 
paralysis is known as monoplegia. 

Cortical monoplegias correspond, as pointed out in the section on 






774 THE NON-NEURONIC DISEASES 

Cerebral Localization, with the particular centers involved in the lesion. 
But these centers have their cell processes bunched together, like the 
stem of a bouquet, in the internal capsule and so on down to the ter- 
mination of the pyramidal tracts in the medulla and cord. Obviously 
the farther down below the cortex the given lesion of the same size 
is located, the more extensive will be the paralysis on the opposite 
side of the body. If the lesion is in the internal capsule, for instance, 
where the bundle is probably as compact as anywhere, the entire oppo- 
site half of the body will be paralyzed. This is known as hemiplegia. 
If both hemispheres or their tracts are diseased, the hemiplegia will 
be bilateral. This condition is termed diplegia. Between a hemiplegia 
and a monoplegia, it is clear that we can have any extent of palsy, 
according to the particular location of the lesion. 

Hemiplegia then is the great, characteristic type of cerebral paraly- 
sis. It involves the entire half of the body. For this reason it is some- 
times spoken of as the facio-brachio-crural type of paralysis. The in- 
ability is most pronounced in those muscles and parts of the body that 
subserve the higher, complicated voluntary movements. There is a 
direct ratio between the degree of intelligence involved in the normal 
movements and the degree of palsy which they have now undergone. 
For this reason the hand is more affected than the foot, the arm more 
than the leg, the arm and leg more than the face, the tongue and lower 
part of the face more than the upper part of the face, and the upper 
part of the face more than the great truncal muscles. 

With the evolution of human intelligence and brain power there 
is a constant tendency to separate the actions of the two sides of the 
body. This is shown in the remarkable feats accomplished, as the re- 
sult of practice, by pianists which ordinary mortals cannot do. It has 
been .intimated that in time we may move each eye without regard to 
the other. At all events, it is a fact that the great tendency in cere- 
bral evolution is towards the separation of the functions of the hemi- 
spheres. In those movements in which this separation has reached the 
highest degree at the present time, disease of one or other hemisphere 
will be most marked. Where, however, the movements are bilateral 
still, as they are in the movements of the eyeballs and the apparatuses 
of sound, deglutition, and respiration, the paralysis is not so evident 
because the unaffected hemisphere takes up in part the duties of the 
diseased hemisphere. In other words, the bilateral representation of 
these latter movements in the two sides of the brain is more positive 
than it is of the former movements. In bilateral lesions, however, the 
laryngeal, deglutitory and masticator)' are affected and we have what 
is termed pseudo-bidbar paralysis. Of the trunk muscles, the trape- 
zius is affected as a rule, though the sterno-mastoid aets normally. In 
a deep respiration, the paralyzed side expands somewhat less than the 
other side. 

The cases in which hemiplegia has occurred on the same side as 
the lesion are open to grave doubt. Most of them were diagnosed be- 
fore our knowledge of the central nervous system was as exact as it 
is to-day. Pressure by contrecoup or lesions in the opposite hemisphere, 
or in the pons and medulla, were not taken into account. However, a 



THE NON-NEURONIC DISEASES 

FIGURE 187. 



tE G 



775 




— Diagram of motor path from right brain. The upper segment is black, the lower 
The nuclei of the motor cerebral nerves are shown on the left side : on the right 
side the cerebral nerves of that side are indicated. A lesion at 1 would cause upper 
segment paralysis in the arm of the opposite side — cerebral monoplegia ; at 2, upper 
segment paralysis of the whole opposite side of the body — hemiplegia; at 3, upper 
segment paralysis of the opposite face, arm, and leg. and lower segment paralysis 
of the eye muscles on the same side — crossed paralvsis; at 4, upper segment paraly- 
sis of opposite arm and leg, and lower segment paralysis of the face and the external 
rectus on the same side — crossed paralysis: at 5, upper segment paralysis of all mus- 
cles below lesion, and lower segment paralysis of muscles represented at level of 
lesion — spinal paraplegia; at 6, lower segment paralysis of muscles localized at seat 
of lesion — anterior poliomyelitis. (Van Gehuchten, modified.) 



Jj6 THE NON-NEURONIC DISEASES 

congenital absence of the pyramidal decussation, a developmental 
anomaly, is assumed in explanation of these homolateral hemiplegias. 

The gait of a hemiplegic is characteristic. The leg remains weak 
and is dragged by the patient. The extensors of the foot and toes 
remaining paralyzed, the equino-varus attitude is assumed and the 
toes not being lifted off the floor, the foot is scraped outward in a 
half circle each time it is moved forward. The flexors of the knee are 
apt to remain paralyzed also. In the arm the palsy remains in the 
hand and fingers, the movements of the shoulder and elbow being par- 
tially regained. 

Though the paralysis is voluntary, the muscles act under certain 
conditions. Under strong emotion, gesticulation and in associated 
movements this is often the case. Automatic and reflex functions they 
still retain. 

The psychic or mental paralysis of Krafft-Ebing and Bruns is 
due to the dissociation between the cortical sensory and motor elements. 
Upon request the patient moves his limbs but not of his own purpose 
or desire. 

Contractures, early and late, usually follow the cerebral palsies. 
The former develop in the first few hours or days after an apoplectic 
stroke; whereas the latter appear many weeks later, never before two 
weeks from the onset of the trouble. The former is due to an irrita- 
tion of the pyramidal tracts ; the latter are not clue to, though they pro- 
ceed in order with, the corresponding secondary degeneration in the 
pyramidal tract. Adduction, flexion in the arm, pronation in the hand, 
and flexion in the fingers occur. The leg is extended and the foot, as 
I have stated above, is in the attitude of equino-varus. The increase 
of the contracture by sensory stimulation, especially cold, electricity, 
etc., its disappearance in sleep, and other factors indicate that it is un- 
doubtedly due to the slight overaction of the lower motor segment 
when the inhibitory power of the upper segment is weakened. This 
explains, of course, the association of an increased action of the deep 
reflexes with these contractures. In some cases there is a slight wasting 
of the muscles from non-use but no true atrophy. What atrophy there 
is, is probably due to the absence of the normal nervous impulses, 
which in themselves are somewhat stimulating to the nutrition of the 
muscular tissues. In every hemiplegic there is some weakness in the 
unparalyzed side. 

Associated movements not infrequently occur in the paralyzed 
limbs. If the patient, for instance, grasps vigorously with his well 
hand or suddenly raises his unaffected arm, the same movement will 
be partially performed in the paralyzed hand and arm. 

The changes of a trophic nature that are occasionally observed 
in and about the joints of hemiplegics are supposed to be due to neuritic 
or consecutive myelitic changes and not directly to the defeneration 
in the pyramidal tract. 

Alterations of local temperature, sweating, (edema, redness, etc., 
in the paralyzed limbs are sometimes noted and may be due to vaso- 
motor disturbances in the cortex. 

Hcmichorea. — As a post-henuplegic phenomenon this is not un- 



THE XOX -NEURONIC DISEASES JJJ 

common ; as a pre-hemiplegic one it is rare. According to Charcot it 
is due to a slow, progressive hemorrhage in the optic thalamus, irritat- 
ing the pyramidal fibres where they course through the internal cap- 
sule. The movements are jerky, irregular and incoordinated just as 
they are in any, chorea. The whole side or extremity is usually in- 
volved. 

Athetosis. — In the fingers and toes occur, after hemiplegia, espe- 
cially infantile hemiplegia, curious, wavy, involuntary movements, that 
are the result of irritation of the pyramidal tract. The fingers undergo 
continuous polyp-like slow extension and flexion, adduction and ab- 
duction. They occur in sleep ; sometimes only upon voluntary move- 
ment. The fingers are moved separately, causing a most grotesque 
and bizarre appearance. Opposite movements are made in adjoining 
fingers simultaneously sometimes. 

Other movements of irritative origin that are neither choreic nor 
athetoid are also seen in conditions of hemiplegia. Among these may 
be cited the associated movements referred to above, unilateral tremor 
and movements similar to those of paralysis agitans and disseminated 
sclerosis. 

Alternate Hemiplegia. — When the pyramidal tract is damaged in 
the lower part of the pons, just after the central facial tract has decus- 
sated, the paralysis will be in the face on the same side as the lesion 
but in the limbs on the opposite side. In an alternate hemiplegia, the 
hypoglossus may be paralyzed on one side and the extremities on the 
other. The tongue will then protrude toward the sound side. 

Conjugate Deviation of the Head and Eyes. — This is often seen 
as a symptom of brain disease. In cerebral lesions the deviation is 
toward the unparalyzed side, or towards the side of the lesion. The 
muscles that draw the head and eyes toward the hemiplegic side arc. 
of course, weakened as the other muscles on that side are. Spastic 
conditions naturally cause the deviation to be in the other direction or 
toward the spastic side. The reason is obvious. Lesions of the pons 
often deviate the eyes toward the side opposite the lesion, the location 
of the latter being in the common center for the abducens of the same 
side, and the internal rectus of the opposite side. 

Sensory Symptoms. — All qualities of sensation may be impaired 
in intra-cranial disease, especially the senses of touch and position. 
Hemianesthesia j rarely complete, occurs with lesions in the cortical 
motor areas. When the sense of position is disturbed the lesion is 
thought to be in the parietal lobe, though there arc strong grounds for 
believing that this disorder originates from disease limited to the cen- 
tral convolutions. In monoplegias the motor and sensory phenomena 
are confined to the same parts. Sometimes the cortical motor zone and 
other parts of the cortex can be destroyed without 1<>^ of sensation. 
Wernicke and ( )ppenheim claim they have observed a tactile paraly- 
sis that Is a mental anaesthesia. With the sensibility intact in tin- hand. 
objects could not be recognized by touch. (See my views upon this 
subject under the head of psychic .symptoms, localization centers and 
psychic blindness. ) 

Hemianesthesia occurs on the side Opposite that of the cerebral 






778 



THE NON-NEURON1C DISEASES 



FIGURE 188. 





Position of the fingers in athetosis. (After Strumpell. 






THE XOX-XEUROXIC DISEASES 779 

lesion. It involves the entire skin and mucous surfaces of one-half 
of the body when it is complete. Grasset claims that the cornea is in- 
tact but that is hardly probable. The immediate cause of this symp- 
tom is, of course, damage to the sensory conducting tracts. Cortical 
hemianesthesia is rare. The course of the sensory tracts have been 
traced in the description of the anatomy of the brain. 

The anaesthesia is not always the same in all parts of the affected 
side of the body. It will sometimes be more marked in one place than 
in another. All forms of sensation may not be equally involved. 

Hemianaesthesia is often accompanied by impairment of the spe- 
cial senses, the two sets of pathways being contiguous. Hence with it 
there may be hemianopsia or crossed amblyopia. Crossed anccsthesia 
occurs in upper pontile lesions, the fifth nerve being affected on one 
side and the path from the limbs on the other. Pontile disease also 
.sometimes causes incomplete bilateral anaesthesia. 

Sensory irritation or pain in the limbs often occurs when the sen- 
sory tracts are only partially destroyed. Sometimes under these cir- 
cumstances numbness, tingling and other paraesthesiae are observed. 
These, cannot be determined as tract or cortical symptoms. 

Ataxia sometimes occurs m the opposite extremities from disease 
of the sensory cortex and the conducting tracts. 

In hemiplegia and hemianaesthesia there are apt to be vasomotor 
and trophic symptoms. In the affected limbs the cutaneous tempera- 
ture is lowered, the parts are reddened, or cyanotic and ©edematous. 
In severe cases a tendency to decubitus is present. Skin eruptions, 
falling of the hair, and even gangrene have been observed. Slight 
arthropathy may occur. 

Olfactory Symptoms. — In examining the sense of smell we are 
wholly dependent upon the subjective testimony of the patient. When 
the olfactory nerves are affected by way of the anterior nares we call 
the sensation an odor ; when by way of the posterior nares, it is termed 
a flavor. As the nares are innervated by the trigeminal as well as by 
the olfactory nerves, the examination must be made with substances 
that affect only the latter nerve, such as musk, asafoetida, oil of cloves, 
oil of peppermint, oil of lavender, oil of turpentine. The substance 
is simply held under one nostril, while the dther nostril is closed. Am- 
monia and acetic acid irritate the filaments of the fifth nerve in the 
mucous membrane. The sense in the two nostrils should be com- 
pared and the intelligence of the patient in regard to the subject o: 
odors must be given due consideration. There is an olfactory reflex. 
Disgusting odors cause the head to be drawn away and the mouth to 
be retracted. For a description of the ol factor) apparatus, the section 
on the anatomy of the brain should be consulted. 

Anosmia or the loss of the sense of smell may. of course, occur 
from local disease of the mucous membrane. As a symptom of brain 
trouble it may be due to various traumata, disease- of the hones, tumors 
in the anterior fossa of the skull, local meningitis, syphilitic or other- 
wise. Olfactory neuritis, like optic neuritis, may accompany brain 
tumor. Anosmia has been seen in tabes and as the result of primary 
atrophy in old age. It may he bilateral or unilateral. As a eongeni- 



w 






780 



THE NON-NEURONIC DISEASES 



tal condition it is observed in idiots. It resulted once from congeni- 
tal absence of the olfactory nerves. Hereditary anosmia has been re- 
ported. 

Hyperosmia, or olfactory hyperesthesia, occurs in hysteria and 
insanity. It is largely a psychosis in the olfactory sphere. It is not. 
of much clinical importance. 

Olfactory parcesthesice and hallucinations occur. They have been, 
seen as aurae in focal epilepsy when the lesion was in the temporo- 
sphenoidal lobe. They are not common at all. 

Optic Symptoms. — The optic apparatus is a part of the brain,, 
as I have explained in the section upon anatomy. It extends from 
the cornea in front to the occipital cortex behind. The neural part 
includes that from the retina to the cortical area in the cuneus. The 
symptoms of disease in this long tract are of the greatest neurological 
importance. They group themselves naturally under the two heads of 
visual disturbances and ophthalmoscopic alterations. Both of these 
sets of symptoms may be examined objectively but the latter are more 
accurate than the former because they are absolutely unrelated to the 
patient's consciousness. Among the former are various alterations- 
in the field of vision, chief of which are concentric contraction of the 
field, scotomata and hemianopsia. Psychic blindness will be included 
in the discussion of these visual symptoms. Chief among the fundus- 
changes, seen through the ophthalmoscope, are the so-called "choked' 
disc" or optic neuritis, and optic atrophy. 

Visual Disturbances. — In examining a patient's vision for neu- 
rological purposes, it is incumbent to search for refractive and other 
errors, though this belongs especially to the province of the ophthal- 
mologist. In certain nervous conditions such as the unstable neu- 
roses, ocular defects may, as exciting causes, set up headache and 
other symptomatic troubles. These having been eliminated, the visual 
disturbances are to be attributed to an intracranial disorder of some 
sort. We cannot always distinguish by these visual signs optic nerve 
from cerebral disease but in regard to some of them we can draw air 
but conclusive inferences. 

Pupillary reflex disorders may be due to optic nerve disease and 
hence the pupils should always be examined also. The discussion of 
the pupillary phenomena naturally falls under the head of disorders of 
the third nerve. 

Concentric Contraction of the Visual Field. — The determination 
of the outer limits of the field of vision for each eye is accurately made 
with a perimeter. This is not the place to give a minute description of 
this apparatus and the manner of using it. For that the reader should 
consult works upon ophthalmology. Suffice it to say. however, that 
it consists of a semicircular arc or band which revolves upon a center, 
so that it can be placed in the direction of any meridian. This arc is 
divided into degrees from zero at the center to ninety at cither cud. 
By means of a head rest the patient is enabled, with one eye covered, to 
place the other eye in such a position as to fix its gaze upon a small 
object at the center of the arc. While the gaze is kept thus fixed, a 
small white object is slid from the outer end of the arc towards the 



THE NON-NEURONIC DISEASES 781 

center. The moment the patient declares that he sees it, the degree 
on the scale is noted and marks the outer limit of the field of vision in 
that meridian. The process is repeated for all meridians and the de- 
grees jotted down on a chart upon which the normal or average visual 
field is indicated. By connecting these several points on the chart 
with a continuous line, the visual held of the patient is seen at a glance 
-and can be compared with the normal field. 

When the white object, moving on the arc, appears blurred or 
•disappears entirely, there is a defect in the field which is termed a 

FIGURE 180. 




Normal field of vision. B, blind spot of Mariotte. 

scotoma. The head of the optic nerve, known as the blind spot of 
Mariotte, and situated about 10 degrees to the outer side of the fixa- 
tion point, furnishes a physiological scotoma. 

Instead of white, little objects of different color may be em- 
ployed and thus the color fields be taken and compared. The perimeter 
shows that normally the field for green is the smallest. Then follow 
in order, from within outwards, red, yellow and blue. 

It should also be noted that the field of vision is more extensive 
-externally than it is internally. The outer part of the retina is less 
sensitive than the inner, and the bridge of the nose cuts it off some- 
what. As considerable variations in the field are observed normally, 
in every case of unilateral alteration where accurate results are desired, 
the normal eye should also be examined perimetrically at the same 
time. 

In the absence of a perimeter, a rough examination of the fields 
may be made in the following manner. Place the patient with his 
back to the window. Take a seat directly in front of him at a distance 
of about three feet. Cover the eye of tin- patient that is not to be ex- 
amined with a towel. Ask him to lix his gaze steadily upon the oppos- 



782 



THE NON-NEURONIC DISEASES 






ing eye of the examiner. The latter then closes his other eve and at 
the same time brings his ringer along the different horizontal and ver- 
tical lines into the field of vision, holding it about half way between 
himself and the patient. For the color fields a small piece of green, 
red or blue paper on the end of a pen-holder may be substituted for the 
finger. As the finger or bit of colored paper is gradually moved from 
above, from below, or from the side towards the mutual visual 
axis, the patient is told to say when he first sees it. If the patient 
and examiner see it at the same moment at all points in the edge of 
the field, the latter is normal. If the examiner sees it in this line or 
that before the patient does, there is a defect at that point in the pa- 
tient's visual field. 

A concentric contraction of the fields of vision may take place in 
conditions of functional weakness, like hysteria and neurasthenia, from 
simple repetition of the test or from the attention being directed to them 
for a short time. This is even more marked when there is a patholog- 
ical contraction present. This is not a retinal but a central phenome- 
non, for if the contraction is thus produced in one part of the field of 
one eye, the corresponding part of the field of the other eye will be 
seen to be similarly affected. 

When the white fields are contracted, the color fields are as a rule 
correspondingly reduced, so that it may be said that a generally con- 
tracted field is a normal field in miniature merely. 

Sometimes there is no contraction in the white field while the 
color fields are markedly reduced. The color perception is generally 
more easily blurred or destroyed than is the white. As a rule it is only 
necessary to test the green and red fields as they are the smallest and 
undergo the most diminution in morbid states. It must not be forgotten 
that concentric contraction may occur slightly in myopia, myosis, 
paresis of accommodation and with opaque corneal spots. These being 
eliminated as possible causes, we find that this phenomenon is to be re- 
garded as a sign of disease in the retina, optic nerve or brain. 

Loss of sight anywhere within a visual field is spoken of as a 
scotoma. Scotomata may be variously situated and of all shapes and 
sizes. They may be central or peripheral. Concentric ring scotomata 
occur in hysteria. They are organic or functional in origin and may 
therefore be due to variously located lesions in the optic apparatus. 
They may invade the color fields as well as the white. In toxic ambly- 
opia both eyes are affected and the patient complains of misty vision, 
which is due to a central color ( relative) scotoma, especially for red 
and green. The fixed point is a favorite site for scotomata. The peri- 
meter aids one in detecting scotomata, as I have already pointed out. 

Definite geometric defects in the visual fields are usually classed 
under the head of hemianopsia. This is generally a bilateral blurring 
of the half-fields, though it may be unilateral. It is easily enough ex- 
amined. Often the patient is all too aware of it himself. All the ex- 
aminer has to do is to introduce from different sides some small white 
or colored object into the visual field of each eye. lie may use the 
perimeter if he wishes to accurately outline the intact part of the field. 
A most remarkable defect that has been seen several times is that of 



THE NON-NEURONIC DISEASES 783 

hemianopsia for colors without any change in the white field. Usually 
of course the color fields are affected in correspondence with the white. 
This will be referred to again. 

In hemianopsia the dividing line between the dark and light part 
of the field generally passes through the fixation point in the center. 
It may be horizontal or vertical. In this way we have horizontal and 
vertical hemianopsia. The former is almost always due to retinal 
lesions, such as embolism, injuries, etc. In vertical hemianopsia the 
central or dividing line generally passes a little to one side or around 
the fixation point, leaving the central vision very acute. This vertical 
hemianopsia is spoken of as temporal when the temporal halves of the 
visual fields are dark, indicating anaesthesia in the nasal halves of the 
retinae ; as nasal when the inner or nasal halves of the fields are ob- 
scured, denoting anaesthesia in the outer or temporal halves of the 
retinae; as lateral or homonymous in which physiologically similar 
halves of the field are darkened, as for example the temporal half- 
field of the left eye and the nasal half-field of the right. An incom- 
plete hemianopsia may be sector-like and involve only a quadrant, or 
even less, of one or both fields. 

Of all forms of hemianopsia the vertical are the most frequent. 
Xasal hemianopsia is exceedingly rare and is of small practical inter- 
est. There is much doubt overhanging the inferior and superior hemi- 
anopsias. 

In addition to the above conditions, the vision should always be 
tested in regard to its acuity, for which purpose test types are em- 
ployed, and for the perception of color, for which variously hued wools 
are employed according to the method devised by Holmgren. For 
details in regard to these tests works upon ophthalmology should be 
consulted. Every neurologist should be familiar with the use of the 
ophthalmoscope. The ophthalmoscopic alterations are among the most 
important symptoms that we have of intracranial disease. The head of 
the optic nerve is exposed to direct observation at the fundus of the 
eye and as this so-called nerve is really a part of the brain, in observ- 
ing its changes we are observing the brain itself, as it were. 

I will now discuss the localization phenomena of the optic ap- 
paratus, taking up the parts of the latter in an orderly way from the 
optic disc backwards, and note, as far as our present knowledge per- 
mits, the relationship between the special symptomatology and the site 
of the lesion. 

What may be called associated changes in the eye, discoverable 
with the ophthalmoscope, may at times be most helpful in diagnosing a 
brain disease. These changes are not due to the brain trouble but are 
merely collateral manifestations of a much more general trouble, of 
which the brain is the seat of other manifestations. For instance, 
syphilitic choroiditis or tubercles of the choroid may confirm the di 
nosis of brain syphilis or tubercular meningitis. Albuminuric retinitis 
is associated with an arterial degeneration that not infrequently 
eventuates in a cerebral hemorrhage or thrombotic encephalomalacia. 
Miliary aneurisms and vascular lesions of tin brain may legitimately 
be surmised when the same conditions are observed in the retina. 






7«4 



THE NON-NEURONIC DISEASES 






Hemorrhages in the retina and in the pia mater have been seen to- 
gether in severe anaemia, purura, leucocythaemia, albuminuria, gout, 
ulcerative endocarditis and septicaemia. Degeneration of the brain 
sometimes is accompanied by simple atrophy of the disc. 

Neuro-retinitis and optic atrophy are the chief ophthalmoscopic 
changes observable in disease of the brain, because they are consecu- 
tive to and dependent upon the latter. 

Optic neuritis, papillitis, neuro-retinitis, choked disc are all differ- 
ent names for the same pathological process so far as the optic disc 
is concerned. A difference of degree may be represented by the terms 

FIGURE 190. 




Normal Fundus Oculi. 

papillitis and choked disc, but the underlying process of both is es- 
sentially the same. 

As everyone knows from his anatomy the optic nerve enters the 
back of the eyeball through an opening in the sclerotic coat. Its fibres 
bend at right angles like the rays of the sun and spread out on the 
retina. That part of the nerve which we behold in the fundus as the 
blind spot is the papilla. With the ophthalmoscope we can see through 
the translucent, radiating optic nerve fibres the circular edge oi the 
disc. The surface of the disc is not uniform. It has usually a "physio- 
logical cup" in its center which is rather pale from the scarcity or 
absence of bloodvessels in it. The periphery of the disc is more 1 
cular and hence more rosy in tint. Simple congestion of the dis< 
rare and of little importance. Much more significant is the swelling 
of the papilla and diminished translucencv which it exhibits when there 
is an actual pathological change. With such a change, the edge of the 



THE N0N- NEURONIC DISEASES 



7*5 



disc becomes blurred and finally entirely obscured. The dis- 
tinctness of the outline of the disc, as affected by a morbid change, 
undergoes greater modification under the direct than under 
the indirect method of examination with the ophthalmoscope, 
Gradually the change involves the entire circumference of 
the disc ; the swelling obliterates the central cup with a 
mere trace of a depression left ; and the vessels, as they course down 
the sides of the enlarged papilla, diminish or disappear from view 
because the plane of their reflection has ceased to be at right angles 

FIGURE 191. 




Optic neuritis (choked disc) in cerebral tumor. (After Gowers.) 



to the line of the examiner's vision. The entire papilla assumes a red 
or grayish red tint, increases to two or three times its normal diameter 
and exhibits in its surface spots which are the accumulations <»i" tin- 
products of degeneration. Early in the process the vessels are little 
altered but soon the veins become swollen, the arteries narrow and the 
blood extra vasated. 

The rapidity of the process varies in different cases. In a feu- 
days the swelling may increase and measure six or more diopters from 
its blurred base to the apex. We speak of it as choked disc when '1 
measures as much as two diopters. The change may reach a very 
high degree of intensity in a couple of weeks, or it max si ill he chronic 




786 



T 1 1 E X ON- N E U RO X I C DI SE A SES 



and moderate after several months. Quick developments of the disease 
usually mean high intensity of it. 

When the papillitis subsides the arteries become more contracted, 
the veins diminish in size, and the swelling after lingering awhile slowly 
settles back revealing once more the edge of the normal disc. Unless 
the neuritis has been very moderate, some permanent alterations re- 
main, consisting of new tissue, with a white and atrophied appearance 
and associated damage to the neighboring edge of the choroid. This is 
sometimes called consecutive, or neuritic, atrophy. The retina in 
severe cases may have its nutrition affected, especially near the macula, 
and this leads to an appearance in it much like that of albuminuric 
retinitis. 

Under the microscope, the papilla presents in its diseased state 
all of the usual changes observed in neuritic inflammation. 

The anatomical cause of choked disc, as it is seen for instance 

FIGURE 192. 










Section through a "choked' 
Randall.) 



disc in brain tumor. (After de Schweinitz and 



in brain tumor, is obscure. It may be due to one or more conditions. 
It is without doubt in the beginning a pure oedema of the nerve head 
as a part of the inflammatory process going on inside of the cranium. 
Whether this oedema is a mere mechanical product, due to compres- 
sion or the carrying of the increased subdural and arachnoid fluids 
along the channels of the nerve to the papilla, or to the irritating toxic 
qualities of that fluid, or to both causes combined, we do not know 
positively. The probability is that the neuritis is due to the descent 
of the irritative influence which, when it reaches the papilla, sets up 
an intense inflammation. This is aided by the retention of the inflam- 
matory fluids, carrying irritating material, on account of the distention 
of the sheath. A chronic intracranial disease may cause an acute 
optic neuritis but a chronic neuritis never follows an acute brain lesion. 
There is a parallelism between the chronicity of the neuritis and that of 
the cerebral disease. Subsidence of the brain trouble is usually ac- 
companied by lessening of the neuritic trouble. Thus we can follow, 
by direct observation to a certain extent, the progress of the intra- 
cranial disease. 




PLATE Til. 



Optic neuro-papillitis in a case of known cerebral tumor. 
Drawn from life. ' After Beard. 



THE XOX-XEUROXIC DISEASES 787 

The vision is often but little affected in the presence of choked 
disc. When the process is advanced, however, the visual fields are con- 
tracted and there is a diminution of the central acuity. Complete 
amaurosis sooner or later occurs. Sometimes the blindness appears 
abruptly, remains awhile and disappears with equal suddenness. This 
has been explained on the basis of a periodic increase in the intra- 
cranial pressure. 

Among the causes of choked disc are to be noted especially brain 
tumor (occuring in 70 per cent, of all cases of tumor), internal hydro- 
cephalus, cerebral abscess and sinus thrombosis. Optic neuritis also 
occurs occasionally in cerebral hemorrhage, anaemia from loss of blood, 
diabetes, albuminuria, acute infectious fevers, saturnine encephalo- 
pathy. More rarely it has been seen in acute non-purulent encephalitis. 
It is not uncommon in brain syphilis and basal meningitis. Hemorrha- 
gic pachymeningitis, ulcerative, endocarditis, and certain cranial 
anomalies such as oxycephalic have been accompanied by it. There 
is said to be a rheumatic optic neuritis. 

Optic atrophy usually follows continued optic neuritis. There are 
two forms of atrophy recognized clinically. Primary optic atrophy, 
as is seen in dementia paralytica and in disseminated sclerosis, tabes 
and perhaps rarely in some cases of syphilis, is an associated condition 
and is not a direct proof of intracranial disease. It is distinguished 
by marked pallor, the border of the papilla being more sharply de- 
fined than it is normally. Great variations are possible, however, so 
that a diagnosis from ophthalmoscopic appearances should be made 
cautiously and only after repeated examinations. 

Secondary, or consecutive optic neuritis, follows brain disease 
such as tumors, wounds, bone diseases, etc. Unlike primary atrophy, 
it is more frequently unilateral. The visual disturbance then precedes 
the eye-ground changes. 

The vision of course is lost in optic atrophy. In disseminated 
sclerosis it is rarely a complete loss, however, or lasting. Amblyopia 
accompanies partial atrophy, though there may be amblyopia without 
atrophy. Such are some of the toxic amblyopias. These are seen 
as a result of retrobulbar neuritis occurring occasionally in polyneuritis 
and after acute infectious diseases. Chronic alcoholic and nicotine 
poisoning are the principal causes of toxic amblyopia. In some cases 
other causes have been reported, as for instance salicylic preparations, 
chronic lead poisoning, methyl alcohol ("Columbia spirits," Jamaica 
ginger, bay rum) quinine, carbolic acid, carbon disulphide, etc. In 
these cases the visual disorder is bilateral, foggy or misty. There is 
a relatively central scotoma for red and green which extends out- 
ward from the fixation point and includes the blind spot. Central 
visual acuity is diminished. This is all due to an interstitial optic 
neuritis of the papillomacular fasciculus in the optic trunk. Then 
nothing to be seen as a rule with the ophthalmoscope, though there- 
may be a slight pallor of the temporal half of the papilla. A non- 
toxic amblyopia is seen but its cause is unknown. There is als< 
hereditarv form with an absolute central scotoma. Though it is not 



788 



THE NON-NEURONIC DISEASES 



seen in these cases, it is to be remembered that in chronic lead poison- 
ing a progressive optic atrophy and ocular paresis do occur. 

Choked disc, optic neuritis, optic atrophy and toxic amblyopia 
are not very definite as localizing symptoms. In fact they belong to 
the general brain symptoms, though they are more definite than such 
general symptoms as headache, vomiting and vertigo previously dis- 
cussed. 

We have now to discuss the visual manifestations by which lesions 
can more or less be definitely localized in the optic tract. The reader 
is again urged to refer to the chapter upon the anatomy of the brain 
where the optic tracts and their decussation are described and diagram- 
matically illustrated. 

Behind the optic nerve, of whose diseases the etiojogy and symp- 
tomatology we have just been studying and found to be not very 

FIGURE 193. 




Field of Vision in Chronic Lead Poisomnj 
(Nimier.) 



definite as localization signs, we come to the optic chiasm, the optic 
tracts, the primary optic centers in the inter- and mid-brains, the 
optic radiations of Gratiolet and the occipital cortex. The symptoms 
of disease in any of these parts of the optic apparatus are almost en- 
tirely visual. In other words there need not be with them any oph- 
thalmoscopic alterations unless the optic nerve trunk is at the same 
time implicated. A lesion of the chiasm, if of long standing, may. 
however, set up a descending atrophy and thus present a change in 
the appearance of the fundus oculi. 

The chiasm is affected generally by tumors of the hypophysis 
cerebri. Syphilitic and tuberculous growths are not uncommon and 
may be inside or outside of the chiasm. Pressure from a neighboring 
pachymeningitis may affect the commissure. Other sources of dam- 
age are internal hydrocephalus, distention of the infundibulum of the 
third ventricle and vascular lesions such as interstitial hemorrhage 



THE NON-NEURONIC DISEASES 789 

within its mass. It has been diseased in tabetic atrophy and has been 
the seat of an interstitial inflammation. 

If the reader will carefully note the course of the optic fibres 
through the chiasm, he will readily understand a bitemporal hemi- 
anopsia, such as is illustrated in the article on acromegaly in another 
part of the volume. The center of the chiasm being most involved, 
the mesial halves of the two retinae are anaesthetic. Nasal hemianopsia 
is exceedingly rare and of course would be most likely a unilateral 
phenomenon, whereas temporal hemianopsia is practically always 
bilateral. Amblyopia occurs at first but total blindness comes on sooner 
or later from the consecutive atrophy. 

The optic tract behind the chiasm may be injured by tumors at 
the base of the brain on the inner part of the temporo-sphenoidal lobe. 
Softening and hemorrhage occasionally, but rarely, damage the tract. 
Sometimes spots of disseminated sclerosis occur in it. The crura 
cerebri may be implicated at the same time. Within the hemisphere 
the tract is hurt by softening, hemorrhage, tumor and various trau- 
matic lesions. 

A lesion that destroys a tract on one side causes homonymous 
hemianopsia. As I have pointed out elsewhere the line of division in 
these hemianopsias is vertical and does not pass, as a rule, through 
the fixation point. It passes around the latter so that the central 
acuity is not disturbed. There are many variations on this, however. 
The variations are probably due to individual differences in the de- 
cussation of the nerve fibres. There is no special localization valua- 
tion to be attached to these differences in the course of the line of 
division between the light and dark half-fields through or around the 
fixation center. Cowers says he doubts whether the dividing line ever 
passes actually through the fixing point* 

The hemianopsia is not always complete. A quadrant may repre- 
sent the blind area or any sector-like form. This is to be attributed 
to the partial extension of the lesion in the tract or visual centers. 
It is very rare in diseases of the tract where the fibres all lie so close 
together. It has been seen in partial softening. Partial hemianopsia 
is common enough, however, in disease of the occipital lobe. 

In hemianopsia there is always some central amblyopia, even when 
the division is a considerable distance from the fixing point. 

The light half of the fields in hemianopsia usually preserve their 
normal boundaries. Very often, however, they arc contracted some- 
what, even when there is no suspicion of a peripheral or ring neuritis. 

I have already referred to the fact that the color fields are affected 
in hemianopsia in the same way that the light fields are. / /emiaehrom- 
atopsia is a remarkable phenomenon that has been occasionally seen. 
The half fields for color are affected while those for ordinary white 
light are intact. The division line here seems to pass through the 
fixation point. The lesion in this case is probably in the occipital lobe. 
Just where the center that is affected is located in the lobe we do nol 
know. 

Except as hemiachromatopsia (lesion in the occipital cortex) and 
with a contraction of the unaffected half fields (lesion probably in the 










790 



THE N0N-NEUR0NIC DISEASES 



optic radiation near the thalamus), there is nothing distinctive about 
hemianopsia by which we can localize the lesion more definitely than 
to say it is in the optic tract somewhere between the chiasm and the 
occipital cortex. As the connection between the optic tract and third 
nerve occurs in the primary optic centers, Wilbrand and Wernicke 
have tried to make use of this fact in localizing a lesion in connection 
with hemianopsia. If light be thrown on the unaffected half-field and 
the lesion causing the hemianopsia be in front of, or in, the primary 
optic centers, there will be no pupillary response ; but if the lesion be 
behind the geniculate and quadrigeminal bodies, there will be a pupil- 
lary response. This does not work out so well clinically, though 
theoretically it is strictly correct if we are sure of our knowledge in 
regard to the reflex centers in the primary optic nuclei. 

Other symptoms added to the hemianopsia often enable us to 
localize the lesion very definitely. Hemianopsia due to lesions in the 
optic tracts immediately behind the chiasm is usually accompanied by 
other cranial nerve symptoms. If the lesion be in the thalamus or 
external geniculate bodies, the collateral symptoms will generally show 
implication of the internal capsule and be a hemiplegia or hemianses- 
thesia on the same side as the hemianopsia. If the lesion is in the 
left hemisphere, the visual paths are so located that with the hemi- 
anopsia will probably be some speech disturbance. If the lesion is in 
the cortical or subcortical fibres, irritative signs, such as facial hallu- 
cinations which are apparently the only symptoms of an irritating 
focus in the visual center, will appear. 

For obvious reasons, reading is extremely difficult in right-sided 
hemianopsia. The condition, even when slight, is usually recognized 
by the patient, and yet a case is recorded where the trouble was only 
discovered by the nurse noting that the patient never ate the articles 
of food placed upon one side of the plate. Hemianopsia patients usu- 
ally carry their heads turned a little toward the blind side. These 
patients are liable to accidents. 

Bilateral hemianopsia, if complete, necessarily results in total 
blindness. In this way extensive lesions in the optic apparatus behind 
the primary centers cause complete loss of sight. Incomplete bilateral 
hemianopsia, in which central vision is not lost, may not result in total 
blindness, but the orientation, or ability to distinguish things will be 
greatly impaired. Complete color blindness of apoplectiform onset, 
bilateral hemiachromatopsia, has been seen. The ordinary vision was 
not disturbed. 

There are no ophthalmoscopic changes in hemianopsia, except 
what may be attributed to the causative lesion, such as a tumor or 
associated hemorrhage. 

Hemianopsia may be transient or permanent, functional or toxic. 
It is not at all improbable that in some cases of uremic amaurosis and 
lead poisoning, there is a toxic, transient, bilateral hemianopsia of 
cortical origin, for the pupillary responses often remain normal. It 
these are lost too then the blindness is probably neuritic in origin. 
A transient functional hemianopsia may associate itself with the scin- 



THE NON-NEURONIC DISEASES 791 

filiating scotomata of migraine. As an indirect focal symptom, a 
transitory hemianopsia has been seen to follow an apoplectic attack. 

Psychic Blindness. This peculiar disorder was first observed by 
Munk in animals. It has been noticed in man also a number of times. 
Vision is not lost but visual comprehension is gone. Objects, including 
of course, written word symbols are seen but not recognized. There 
seems to be a complete failure of memory pictures in the visual sphere. 
A familiar person, a chair, a street are clearly seen but they seem 
perfectly strange and unfamiliar to the patient. The patient sees with 
his eyes but not with his mind. This psychic blindness is not the 
same as visual aphasia. Munk produced the condition in animals by 
removing the occipital lobes. In man it has usually been associated 
with homonymous bilateral hemianopsia of one side. As it does not 
always occur with hemianopsia, there is doubt about its being a mani- 
festation of an occipital lesion. This is so frankly recognized that 
those who have tried to explain the phenomenon, have adopted the 
notion that there is still a higher visual center, possibly in the anterior 
part of the occipital lobe or lower part of the parietal lobe, that re- 
ceives impulses from the occipital cortex and there gives them their 
higher or psychic interpretation. The existence of this so-called higher 
visual center is not only hypothetical but it is unsupported by the 
slightest shadow of anatomical evidence. It is a sorry makeshift 
from one dilemma into another. 

Psychic blindness is a psychic manifestation and should be classi- 
fied under the previously named psychic symptoms. I mention it here 
because it happens to be a psychosis in the visual sphere. As I have 
stated at the end of the section on the mental manifestations of brain 
disease it is a crude conception of psychological phenomena to think 
that they are subserved by small cortical areas scattered here and 
there throughout the brain. It belongs to the mode of reasoning adopt- 
ed in the phrenology of the long ago. 

Visual recognition is a complicated act. It is the result of a 
combination among a great many elementary psychic sensations. These 
psychic sensations have their physiological counterparts in the pure 
physiological visual sensations that are received by the cortex of the 
occipital lobe. Simple psychic elementary vision may well be conceived 
therefore as having its seat in the occipital cortex. But psychic ele- 
mentary vision is something very much more simple than visual mem- 
ory and visual recognition. These are the result of inter-connections 
between psychical compounds which are themselves made up of 
anatomico-psychic elements. From the very nature of things there 
cannot be a single center for compound, complex psychic phenomena, 
though there may be centers where the various constituent elements 
are brought in touch with one another, or at least in which certain 
physiological inter-connections are established from which start the 
various psychic manifestations. 

The whole doctrine of the cortical centers has up t<> the present 
time been most crudely taught and only now arc we beginning to 
realize that these so-called centers which we have heretofore supposed 
subserved most complicated psychic acts arc merely the starting 






79 2 THE NON-NEURONIC DISEASES 

points, the threshholds, the central clearing houses, as it were, of the 
vast and intricate workings of the mind which for its physical basis 
requires the whole brain with all its enormously inter-connected parts. 

Psychic sensation of the elementary vision may have its seat in the 
occipital lobe. Psychic visual memory and comprehension is probably 
coextensive with all of the brain functions. 

Visual hallucinations are psychic symptoms that happen to be in 
the visual sphere. Closely related to them, if not exactly the same, are 
mcgalopsia, or the apparent enlargement of objects, and micropsia, 
or' the apparent reduction m the size of objects. These may be due 
to displacement of the retinal rods and cones. More often, however, 
they are among the psychic phenomena of neurasthenia and hysteria. 

Monocular diplopia seen in hysteria is a psychosis. True diplopia 
is a visual disturbance caused by paralysis in the ocular motor nerves 
and is mentioned elsewhere. 

Hyperesthesia of the retina, causing photophobia, lachrymation 
and involuntary closure of the eyelids may be due to optic nerve hyper- 
sensitiveness. There is reason to believe that the fifth nerve is at the 
bottom of photophobia. It is a suspicious fact that diseases in which 
photophobia is most marked involve the structures that are innervated 
by the trigeminal nerve. There may be a central inter-connection, 
however, between the optic and the fifth nerves. 

Gustatory Symptoms. — These are easily examined by placing 
various substances on the tongue. The four kinds of taste are sweet, 
sour, salty and bitter. Sugar, vinegar, salt and quinine may be used 
to test each respectively. Disorders of taste are usually due to nerve 
diseases and have been referred to under the head of the trigeminal 
and glosso-pharyngeal nerves. There are hallucinations of taste. 

Auditory Symptoms. — These are tested by whispering, after 
closing the ear that is not under examination, by holding at different 
distances a ticking watch and by sounding a tuning fork. A normal 
person should be employed as a control test. Bone conduction of 
sound is determined after closing the ears by placing the watch, or 
handle of the sounding tuning fork against the mastoid bone or be- 
tween the teeth. Bone conduction is often preserved when the mechani- 
cal hearing is lost. When the nerves and their centers are diseased. 
bone conduction is also lost. 

Rhine's test is an excellent one to distinguish nerve from mere ear 
deafness. In a normal person the vibrating fork, after being placed 
against the bone and no longer heard, is placed in front of the ear. 
Its sound is again heard. This occurs exactly the same way in nervous 
impairment of audition, except when it approaches actual deafness. In 
mechanical impairment, the fork is not heard the second time. 

Weber's is also a good test. Place the sounding fork on the 
frontal bone and it will be heard as it from a distance. The sound 
will be referred to both ears. If one ear is then closed, the sound 
will be referred to that ear. When the same test is made upon a 
patient, if the impairment of hearing is nervous the sound will be 
said to be heard in the well ear ; if it is due to the sound-conducting 
apparatus, it will be referred to the diseased ear. 



THE NON-XEURONIC DISEASES 793 

According to Schwabach the fork on the head is heard longer than 
normally in disease of the conducting apparatus, shorter than normally 
in cerebral impairment of hearing. 

When there is irritability with audition, the condition is some- 
times called acoustic hyperesthesia. Paracusis is where a tone is 
heard deeper or higher than it really is. If the sound ear hears the 
normal tone at the same time, the condition is called diplacusis. 

DISEASES OF THE MEMBRANES OF THE BRAIN. 

The diseases of the intracranial meninges are all essentially in- 
flammatory in type. The origin, course and ultimate results of this 
inflammation may be different in different cases but its essential nature 
is the same in all. It may be so slight, incipient or transient as to 
merely amount to a circulatory disturbance. Anaemia and hyperemia 
may express the entire pathology of the case; on the other hand the 
most violent characteristics of a severe inflammation, simple or puru- 
lent, may constitute the disease process. 

Of the three membranes the dura mater and the pia mater are the 
only ones whose inflammation is of clinical significance. The arachnoid 
is never diseased by itself. 

Ancemia. — This has no clinical existence as a disease by itself, so 
far as we know. In anaemia of the brain, the membranes are also 
anaemic. It cannot therefore be discussed here. 

Hypcrccmia. — Congestion is always the first stage of an inflam- 
mation and consequently has all of its symptoms in a slight or transient 
form. There may be headache, throbbing and full in character, ver- 
tigo, delirium, convulsions, and even coma and death. These fulmi- 
nant cases reveal an intense meningeal hyperaemia, which is perhaps 
better described as a rapid, overwhelming meningitis. The whole or 
a part of the membranes may be involved. When the pia is impli- 
cated, it is a part of congestion of the brain. When the dura is the 
seat of the congestion it has the same etiology and symptomatology 
practically as pachymeningitis. 

PACHYMENINGITIS. 

As the dura mater consists of two layers, a thin, internal, smooth- 
ly epitheliated layer and an external, loose, periosteal layer, either of 
which may be primarily inflamed, we have a pachymeningitis interna 
and a pachymeningitis externa. 

External Pachymeningitis. — This is the most common inflam- 
mation of the dura, (ienerally it is a secondary disease and is asso- 
ciated with surgical conditions. 

Etiology. — Fractures of the skull, blows and other injuries to the 
head, with effusion of blood between the bone and the membrane, are 
the most glaring causes of it. Diseases of the bones of the head, 
caries and necrosis of the petrous, mastoid, ethmoid or outer table 
even of the squamous bones may light up the inflammation. Erysipelas, 
otitis media, ozaena and other disease^ may cause it by extension. 



794 



THE NON-NEURONIC DISEASES 



Syphilis and neoplasms have originated it. As a great rarity it has 
been seen to occur without any traceable cause. For obvious reasons 
it is rare in children. 

Pathology. — The findings of the primary trouble which has 
caused the pachymeningitis are of course a part of the pathology. 
The dura itself exhibits all the changes of a purulent inflammation. At 
first it is congested, red, cedematous and later on infiltrated and bathed 
in pus which flows and accumulates between it and the bone. Oc- 
casionally the purulent matter extends between the two layers of the 
dura and even into the arachnoid beneath it, setting up a purulent 
dura-arachnitis. The pia may become involved and all the membranes 
be glued together or bound by adhesions. Sometimes the inflammation 
goes down without the appearance of pus, in which case it often be- 
comes firmly attached to the skull and is penetrated by osteophyte 
growths. In syphilitic cases the bones may be greatly thickened, the 
pus large in quantity and the membrane itself in a very rough and 
almost sacculated condition. 

Symptoms. — These are indefinite because they are obscured by the 
symptoms of the primary disease and because the lesion is so out- 
stretched and variable. The discovery of the original cause will often 
enable the diagnostician to determine which of the mass of symptoms 
present are to be attributed to the meningitis. Usually there is a 
gradual onset of headache, fever and delirium. There are compres- 
sion symptoms, especially of a hemiplegic type if the motor cortex is 
implicated. Therefore convulsions and paralyses are to be looked for. 
Focal symptoms are rare. I once was able to follow the extension 
of the brain compression by the extension of the clot from the hem- 
orrhage, in the case of a child whom I saw fall several stories and 
fracture its skull. Trephining failed to save life. 

The course of these cases is acute or subacute and is largely due 
to the nature of the primary disease. As a rule the prognosis is serious 
but somewhat better than it is in most of the other forms of menin- 
gitis. 

The treatment is entirely surgical and is largely the treatment 
of the underlying cause. Pus must be evacuated. If there is reason 
to believe that there is no pus present, the treatment of the mem- 
branous trouble is the same as for any meningitis. 

Pachymeningitis Interna. — Pathologists recognize two forms of 
this, the purulent and the hemorrhagic. They are both uncommon, 
especially the former. Some authors, like Osier, speak of a pseudo- 
membranous internal pachymeningitis, though it is not usually recog- 
nized. Osier saw it as a secondary process in pneumonia. Purulent 
internal pachymeningitis has been seen, very rarely, however, as a 
primary condition. Generally it is secondary to purulent inflamma- 
tion of the pia or dura. Hemorrhagic internal pachymeningitis is a 
most interesting and remarkable disease and is still a subject of much 
debate among pathologists. Some writers classify it among the intra- 
cranial hemorrhages while others still continue to regard it as a men- 
ingeal inflammation. 

Pachymeningitis interna hemorrhagica. Hematoma of the Dura 



THE NON-NEURONIC DISEASES 795 

Mater. Meningeal Blood Tumor. — This is a rare disease of the dura 
mater, characterized especially by the formation of an inflammatory 
membrane with hemorrhagic effusion upon its under surface. Whether 
the hemorrhage or the membranous deposit takes precedence in the 
disease process is the question that is still being debated. I am in- 
clined to think that the disease is primarily a meningitis of a particular 
type and that the hemorrhage is a secondary accident, as it were. 
According to Gowers, Prescott Hewitt., as far back as 1845, described 
the trouble as primarily a dural hemorrhage. Virchow studied it 
anew and in 1854 demonstrated that the origin of it was a particular 
variety of pachymeningitis. This explanation satisfied the medical 
world until Huguenin recently revived Hewitt's hypothesis and ad- 
duced some evidence in support of it. As the question is still sub judice, 
the disease will continue to be classified by authors in accordance with 
their individual confidence in the proofs of one view or the other. 
Etiology. — The disease is very rare in general practice. It is a 
secondary condition and most of the cases are seen among the insane 
in the asylums. It seems to be consecutive to some forms of chronic 
insanity, especially chronic dementia, general paresis, senile dementia, 
chronic mania, chronic melancholia and chronic epileptic psychosis. 
It has been seen to follow acute mania and imbecility, chronic alcohol- 
ism and Huntington's chorea. Most of these diseases, it will be 
noticed, are chronic inflammations and atrophy of the cerebral tissue. 
It has occurred secondarily to certain vitiated and cachectic blood 
states, such as is seen in profound anaemia, in hemorrhagic purpura, 
certain acute fevers like rheumatism and smallpox, in scurvy, leukemia, 
and rarely syphilis. It may be observed in a mild form in renal dis- 
eases, chronic heart troubles and phthisis. Traumatic injuries to the 
head may cause it. It may occur as a primary trouble also. 

Males are subject to it more than females. It is so comparatively 
frequent in old age, especially with mental breakdown, that it is sup- 
posed to be in part at least the expression of physical deterioration 
as much as of actual disease. It occurs in infantile scurvy though as a 
rule it is relatively infrequent in childhood. 

Pathology and Pathogenesis. — The essential feature of dural 
hematoma is the formation of a delicate, vascular membrane on the 
under surface of the dura mater and between it and the arachnoid. 
In about half of the cases this formation extends bilaterally over both 
"hemispheres. In many cases, however, it is limited in extent, spread- 
ing over only one hemisphere or part of a hemisphere. It may occur 
at the base of the brain, in the middle and posterior fossae likewise. It 
is at first a soft red tissue which afterwards becomes paler and harder 
and more compact. It varies in thickness and has a laminated con- 
struction with hemorrhagic extravasation between its six or seven 
layers. Its edges may be adherent and the blood-clot be inclosed in 
a sort of sac arrangement. Sometimes these contain merely a slightly 
-colored serum with crystals of cholesterine. Adhesions between the 
layers of the membrane at a number of places cause it to have a 
cystic appearance. The vascular condition, its rich supply of blood- 
vessels and the degeneration of the extravasated blood, causes the 



79^ THE NON-NEURONIC DISEASES 

ruddy tint in the earlier stages ; while development of delicate fibrous- 
tissue and other organization material are responsible for its later 
firmness and paleness. Not all cases present the same exhibition nor 
does the same case manifest exactly the same changes in all parts of 
the membrane at the same time. In mild cases, for instance, the latter 
may be like a veil or delicate piece of lace, faintly rose-tinted and 
easily pulled off from the dura. The hemorrhages into this may be 
small and punctated, causing spots of brown, brownish-red or yellow 
here and there according to the age of the extravasation. On the other 
hand the disease process may be so violent and elaborate that a thick, 
many-layered, intensely red and hard deposit is made. It may cover 
the brain like a closely-fitting cap and adhere it strongly to the men- 
inges. In such cases it is difficult to pull it away without tearing 
off pieces of the brain substance. The brain next to it is usually 
atrophied. 

Three typical apearances may be noted in the development of 
this hematoma. Some cases clearly show that it consists of a deli- 
cate, inflammatory or organization exudate into which has penetrated 
numerous bloodvessels and much granulation tissue. In other cases- 
there seems to have been nothing but a simple subdural hemorrhage, 
though, as Osier suggests, the membrane may have been in existence 
but was destroyed by the blood. In a third set of cases both vascular 
membrane and hemorrhagic extravasation seem to have been developed 
together. 

It is owing to the fact that the membane thus sometimes appears 
without the evidences of hemorrhage, and that at other times the 
hemorrhagic residua appear without the evidences of the formation 
of a membrane, that so much controversy has sprung up in regard 
to the primary nature of the entire process. Virchow adduced strongs 
proof that the trouble began with internal pachymeningitis, that the 
membrane was nothing but an inflammatory exudate and that the 
presence of the blood was a mere secondary phenomenon. The etio- 
logy and course of the disease, the appearance of the exudate without 
hemorrhagic extravasation in the light cases, and above all the irregu- 
lar distribution and cystic and punctated character of the blood de- 
posits, as though when fluid it found difficult)' in spreading out evenly 
over the surface of the dura, are strong arguments in favor ofVirchows 
view. Hence I treat of the disease as a form of pachymeningitis. It 
must be admitted, however, in all candor that the position taken by 
Huguenin and others is far from being a weak one, namely, that a 
dural hemorrhage takes place and that later on the clot undergoes 
organization and produces all the collateral appearances through irri- 
tation both of the brain and dura. 

Symptoms. — The clinical picture of hematoma of the brain is 
very indefinite, for its symptoms may range from nil all the way to 
those of a profound apoplectic stroke. They are least marked or 
absent entirely in the slight eases, whereas in the traumatic and other 
cases they are both severe and extensive. Ofttimes they are marked 
by the general symptoms of the disease of which the hemorrhagic 
effusion is an accompaniment. This is the ease in general paresis par- 



THE NON-NEURONIC DISEASES 79/ 

ticularly. The seat and character of the lesion, the nature of the 
-associated disease or injury, and the stage at which the disease has 
arrived all determine the general outlines of the symptomatology. 
When a scries of apoplectiform seizures occur, followed by cerebral 
pressure symptoms, in a patient affected with any of the diseases 
known to be causative of hematoma, the latter may be diagnosed. 
Usually the first symptoms are very gradual and insidious, almost 
prodromal, in their onset. A feeling of general distress and restless- 
ness, excitement almost resembling delirium, is followed by an in- 
creasing headache, vomiting, unilateral epileptiform twit chin gs and 
coma. The patient emerges in rare cases from this or he may remain 
in this state for several days or weeks and then die with or without 
another seizure. At times the beginning of the trouble is a genuine 
apoplectic stroke. All of the usual signs appear, coma, paralysis, con- 
jugate deviation of the eyes, contraction of the pupils, retardation of 
the pulse, labored respiration, etc. Vomiting and elevation of the tem- 
perature are not infrequent. All of the symptoms referable to unila- 
teral or bilateral pressure, tollowing a sudden access and showing more 
or less of a progression, may appear in different cases. The hemiplegia 
may be one-sided or double. Both it and the monoplegia are not as 
complete as in ordinary intracranial hemorrhage and are often pre- 
ceded by local spasms and general convulsions. A hemiparesis of one 
side may occur with marked contractures on the other. These are all 
often merely temporary phenomena and may appear with or without 
coma. It is very exceptional for the sensibility to be disturbed. 
Aphasia and nystagmus have been seen in some cases. Choked disc 
is rather a frequent manifestation. The temperature may be subnor- 
mal but it very often goes very high.. 106 degrees F. just before 
death. 

Diagnosis. — This is always extremely difficult. In children it 
is pretty nearly impossible. The chief traits that must be depended 
upon are the presence of injury (these cases usually present the most 
marked clinical presentation) or disease with which hematoma is 
known to occur, a series of apoplectiform seizures occurring like ex- 
acerbations with remissions in a disease that manifests headache, ver- 
tigo, choked disc and other pressure symptoms, temporary or slight 
monoplegia or hemiplegia followed and preceded by spasms, convul- 
sions and contractures. The extensive involvement of the body with 
such paralytic manifestations, not so profound as they are in ordinary 
hemorrhage, would be strongly suggestive of hematoma. 

Cerebral glioma sometimes presents itself in the same way as 
hematoma. The diagnosis is then impossible, though a suspicion may 
be aroused by the presence of some mental or senile condition in which 
hematoma occurs. 

In ordinary meningitis the diagnosis is often very difficult. Haema- 
toma, however, is devoid of nuchal rigidity and cranial nerve < except 
the optic) involvement. In meningitis the remittent character of the 
symptoms, the apoplectic seizures, the choked disc and the intercurrent 
convulsions do not obtain. 

Prognosis. — This is bad. Death usually occurs sooner or later. 



79^ THE NON-NEURONIC DISEASES 

Treatment. — This may have in view the checking of the inflamma- 
tion and the hemorrhages. In neither, however, is it very successful. 
The former suggests free purgation and diuresis, the application of the 
ice bag, leeches and bloodletting in robust individuals. Counter-irrita- 
tion has been tried. To check the hemorrhage has heretofore proved 
to be an impossible task, hence there are no measures to be recom- 
mended beyond those commonly resorted to in intracranial hemorrhage. 

In both traumatic and non-traumatic hematoma, operation has. 
been resorted to with a very fair degree of success. Localization 
symptoms of some degree of definiteness must be present. Dangerous- 
compression of the brain particularly suggests the consideration of 
surgical relief. 

LEPTOMENINGITIS. 

An inflammation of the pia mater includes as a rule the arachnoid 
and the cortex, so that the terms pia-arachnoiditis and meningo-en- 
cephalitis are justified. In most cases it is a diffuse condition, in- 
volving both the vertex and base of the brain and not infrequently 
even the spinal cord. Excepting the tuberculous and syphilitic types, 
the vertex is affected in most of the cases chiefly. The symptoms 
vary in accordance with the location of the disease, but not sufficiently 
so to establish that as a basis of classification. Usually the disease 
is acute, though it may become chronic. It is highly doubtful if it is 
very simple. Most generally it is infective and purulent. Sometimes 
it is specific and epidemic. Its symptomatology is fairly uniform in 
all types. No special classification of it is therefore called for, though 
for convenience sake we may discuss separately Acute (simple and 
purulent) Leptomeningitis, Epidemic Cerebrospinal Leptomeningitis 
and Tuberculous Leptomeningitis. Syphilitic Meningitis is considered 
elsewhere under the head of cerebral syphilis, and serous meningitis is 
referred to under the head of hydrocephalus. It is misleading and in- 
correct to speak as some authors do of the brain condition, the so- 
called "wet-brain," of subacute alcoholism as one of serous meningitis. 
It is not meningitis at all but a mere serous effusion. 

Acute (simple and purulent) Leptomeningitis. — It is very 
questionable whether a simple, non-toxic inflammation of the meninges 
ever occurs. The nearest approach to it would seem to be in some of 
the cases of Quincke's hydrocephalus wherein the ependyma of the ven- 
tricles, and even the cortical meninges, exhibit signs of a low grade of 
pure inflammation. Older writers used to refer to a simple meningitis 
that was caused by insolation, mental strain and simple cerebral con- 
cussion. In some of these cases which succumbed rapidly to death. 
nothing but intense congestion was discovered. This, however, is not 
accepted by many modern pathologists as proof positive of the non- 
purulent character of these cases. They hold that they are merely 
foudroyant cases that do not reach the purulent stage, or arc not cases 
of meningitis at all. Simple non-purulent meningitis is therefore de- 
clared to have no existence. Whether we are yet in a state of knowl- 
edge to adopt so radical a position or not. we are obliged to recognize 
that the vast majority of all the cases of leptomeningitis are of septic 



THE NON-NEURONIC DISEASES 799 

origin. The source and nature of the poison are different in different 
cases. Usually it is an infection carried to the brain from some out- 
side focus by way of the blood. The meningitis is therefore a second- 
ary process except perhaps in the epidemic cerebrospinal form. 

It is convenient to group these various sources of the infective pro- 
cess under several general heads. Traumata, acute alcoholism and 
other depressing influences, and in tuberculous meningitis even 
heredity, exercise an influence as predisposing factors. 

The infective fevers provoke leptomeningitis though not as fre- 
quently as the mere fibrile delirium has led many practitioners to sup- 
pose. It occurs in pneumonia, erysipelas, septicaemia, smallpox, 
typhoid, influenza, measles, mumps, scarlet fever, pyaemia, acute arti- 
cular rheumatism, ulcerative endocarditis, empyema, gonorrhoea, etc. 
The first three give rise to it more frequently than the others. It has 
been ascribed to actinomycosis and is doubtfully associated with in- 
testinal catarrh. The meningitis due. to these causes is practically al- 
ways purulent, though the suppurative process may vary in character 
and severity according to the particular microorganism involved. It is 
an error to refer to this form of meningitis as metastatic. The disease 
is not transferred. The meningitis is simply the expression of a gen- 
eral infection of the organism and may be the only expression. A 
pneumococcus meningitis has been seen without any implication of the 
lungs whatever. 

Injuries and diseases in the bones of the skull, involving the men- 
inges are a not uncommon cause of acute suppurative leptomeningitis. 
The injuries that directly involve the membranes and cause the ordi- 
narv form of pachymeningitis are not referred to here. Fractures, 
blows, concussion may set up a local suppuration with transmission 
of the germs to the pia mater, a sinus thrombosis from the veins of 
the diploe carrying the infection. Caries of the petrous part of the 
temporal bone from otitis media, necrosis of the cribriform plate of 
the ethmoid and disease of the cavities of the skull and their bony 
walls may light up the meningeal inflammation. 

Neighboring foci of suppurative procc esses must also be held re- 
sponsible, such as chronic purulent otitis, mastoiditis, disease of the 
nasal cavity, the orbit, the antrum, frontal sinuses, etc. Then again 
the infection may come in the other direction from an abscess, a 
tumor, an old hemorrhagic or necrotic focus in the brain. An infected 
embolus from an endocarditis is a common cause of the latter. A 
puncture with a sound has carried the disease from the nose into the 
cranial cavity. Vascular sheaths form another path along which the 
poison passes inward ; also the nerve sheaths. 

In certain diseases there is a terminal infection that sometimes re- 
veals itself in a leptomeningitis. It is thus sometimes seen in chronic 
nephritis, gout, valvular and muscular heart disease, senile states, 
arteriosclerosis and the wasting diseases of childhood. 

In some cases the source of the infection cannot be determined 
and the cause of the disease is hidden in obscurity. 

Thus it is made clear that acute leptomeningitis is a bacteriological 



800 THE N0N-NEUR0NIC DISEASES 

disease, a secondary infective process in most cases, with a varied 
etiology. 

The relationship of the disease to age, sex, climate, occupation, 
season and station in life is largely a matter of the original source and 
nature of the primary infection. It may be noted, however, that men 
are slightly more affected by it than are women, and that it is most 
common in children between the ages of one and ten, since during these 
years the infective diseases are most rife and disastrous. 

Pathology and Pathogenesis. — The great pathogenetic fact in 
the development of leptomeningitis is always the presence of disease 
germs or their products. These may be of various types and may be 
the basis of a general or a local infection. Somehow they get to the 
pia-arachnoid membrane and there set up a typical infective or puru- 
lent inflammation. In some cases they have been recovered from the 
diseased membrane post mortem ; in other cases only the remains of 
their destructive work have been seen. It is doubtful if all of the 
germs that are believed to give rise to meningitis will be recovered. 
We are not sure of the exact influence of those that have been so 
far recovered. We dare not yet dogmatize in regard to the relative 
importance of the germs themselves or their biological products. In a 
word, though we have gotten so far as to recognize acute leptomenin- 
gitis as a germ disease, we are still in the dark in regard to many of the 
details. 

Direct examination of the exudate has been rewarded many times 
with the finding of numberless streptococci and staphylococci. Of 
these the former are the more frequently met with. A form of men- 
ingitis that occurs with pneumonia and as an independent affection 
seems to be due to the pneumococcus of Fraenkel. It has been recov- 
ered many times from the membrane. The meningococcus, or diplo- 
coccus intracellularis of Weichselbaum, is in all probability responsible 
for some cases, especially of the sporadic and epidemic cases of cere- 
brospinal meningitis, though in these have been found other bacteria 
also. The pneumo-bacillus of Friedlaender, the typhoid bacillus, the 
colon bacillus, the gonococcus, the tubercle bacillus, and the staphylo- 
coccus have all been isolated from the diseased meninges. 

The streptococcus is the most important in the pathogenesis of 
acute purulent leptomeningitis. It is the germ usually found in those 
cases due to traumata, chronic otitis media, and the septic processes 
generally ; in those associated with ulcerative endocarditis, and those 
due to terminal infection. The staphylococci are found in some of the 
last. 

Purulent inflammation may characterize all parts of the pia- 
arachnoid membrane, though as a rule it appears mostly on the ver- 
tex. It usually covers the entire brain, though it may be unilateral or 
even focal. It assumes the latter form especially in those eases where 
the infection comes from some nearby suppurating focus. It is more 
extensive in the general, infective cases. The pia is at first congested. 
violently reddened, oedematous and cloudy. Gradually a purulent de- 
posit spreads over the sulci, collections of pus appear in spots, unite 
and finally give to the membrane a yellowish, thick, creamy appear- 



THE NON-NEURONIC DISEASES 8oi 

ance. The convolutions are completely hidden. Infiltration takes 
place into the superficies of the brain substance ; small hemorrhages 
occur ; pus deposits in small foci ; and a general encephalitic process 
with some atrophy even may appear. Encephalomalacia and abscesses 
are possible. Very prone is the pus to deposit itself at the base of the 
brain in the Sylvian fissure around the chiasm, beneath the cerebel- 
lum and beside the pons. Sometimes the dura is implicated. In the 
ventricles there pours out a sero-purulent exudate which may so 
distend them that a distinct condition of hydrocephalus is produced. 
The distension is rarely, however, as great as it is in the tuberculosis 
form of the disease. As a very rare condition it is said that a puru- 
lent meningitis may be limited to the ventricles in childhood. A per- 
manent collection of fluid may be left in the ventricular cavities. 

In many cases the spinal meninges are simultaneously affected, 
so that the disease may be truthfully termed a cerebrospinal diffuse 
meningitis. In and about the sheaths of the nerve trunks the purulent 
matter may sometimes be seen. 

Symptoms. — Pathology and practical diagnosis are at logger- 
heads in regard to the frequency of meningitis in the infectious fevers. 
The former finds it very rarely, the latter very often. This discrep- 
ancy is accounted for by the fact that many symptoms of simple con- 
gestion as it occurs in these fevers are like those of a frank menin- 
gitis. Mild delirium, muscular twitchings, spasms and retraction of 
the neck, seen in typhoid fever, for instance, are largely due to the com- 
bined effect of the infection, congestion and elevated temperature 
rather than to an inflammation of the meninges. Post mortem exam- 
inations show that the latter is a very rare complication of the fever. 

The clinical picture of an acute purulent leptomeningitis is a very 
variable one, because it is the result of a general, diffuse lesion of 
infectious origin. Nevertheless there is a sufficient degree of uni- 
formity about it to establish a description of the disease which will 
more or less fit all cases. There are always two sides to it. On the 
one hand are the symptoms that are always characteristic of a general 
infection ; on the other are those that indicate implication of the en- 
tire brain or parts of it. The differences between the various types 
of infection that cause the meningeal trouble produce differences in 
many of the details of the general symptomatology of the infection. 
The differences between the locations of the main foci of inflamma- 
tion in different cases cause a marked variability in many of the cere- 
bral manifestations. 

Some cases appear abruptly while others have distinct prodromata. 
A feeling of general malaise, head soreness, heavy feeling about the 
eyes, vertiginous distress, possibly vomiting, anorexia and general 
irritability and uncompanionableness in a few cases precede for some 
days the outbreak of the signs of inflammation. The prodromata arc: 
more characteristic of tuberculous than of the simple acute menin- 
gitis. The latter as a rule begins somewhat suddenly with a chill, an 
intense headache, a rise of temperature, a rapid pulse and all the usual 
signs of an acute infective process. If these occur in the course of 
the same infective process elsewhere in the body, they will be obscured, 






802 THE NON-NEURONIC DISEASES 

of course, by the symptoms of the general febrile disease. In such a 
case the involvement of the meninges must be determined largely by 
the nature and location of the original source of infection, and its 
probable influence in producing a meningitis, as well as by the more 
definitely localizing cerebral manifestations. 

Among the latter headache easily takes the first rank. It is a 
sharp, excruciating pain that appears with intense exacerbations all 
over the head, though chiefly in the occipital and frontal regions. It 
is never entirely absent, though at times it may undergo a temporary 
recession or remission. It is a persistent, steady pain with sharp, 
boring, knife-like flashes. Even stupor does' not bring relief to its 
victim for in the night when asleep, or later in the disease when the 
comatose condition comes on, he cries out and seizes and grasps his 
head with his hands in manifest suffering. In certain rare cases of 
septicemic meningitis, and others due to blood states, the disease has 
been seen to run its course without, or with only a slight, headache. 

Vomiting, of the cerebral type, is very often present. It should 
be distinguished, if possible, always from the vomiting that some- 
times accompanies the profound alimentary disturbance caused by the 
fever and general infectious disease. It is sudden, projectile and unin- 
fluenced by the presence or character of the food in the stomacn. 

With the headache and vomiting, there is always more or less 
vertigo, especially when the patient moves. Nausea may or may not 
coexist. The bowels are generally constipated and there is flattening 
of the abdomen with a rapid development of an appearance of general 
emaciation. 

Most cases are initiated with a fever which in a few days rises to 
103 degrees or 104 degrees F., sometimes higher. Just before death 
it may go to 108 degrees. It may be masked by the. fever of the pri- 
mary disease. It is an irregular, fluctuating temperature. In some 
cases it may be subnormal, and in a few instances it is normal through- 
out the entire course of the disease. The usual febrile accompani- 
ments such as dry skin, coated tongue, parched lips, all go with it. 

The pulse is rapid, rising to 160 and i"8o before the lethal issue. 
Very often it is slow, even as low as 40 and unsteady. 

The respirations are not often very greatly disturbed. They may. 
however, be rapid, irregular, feeble and suddenly cease. A Cheyne- 
Stokes breathing is a bad omen. Meningitis of the base of the brain 
and particularly in the posterior fossa causes these phenomena most 
markedly. 

The urine is scanty, high-colored and usually contains some albu- 
min. Sometimes sugar is present in it. It is purely a febrile urine 
unless it partakes of the composition of a urine that would be ex- 
pected in the primitive disease underlying the meningitis. The men- 
ingitis of the terminal stages of renal and cardiac affections must not 
be forgotten in this respect. During stupor both retention and in- 
continence of urine may be expected. 

After the headache perhaps the most characteristic symptom of 
meningitis of this type is the delirium. This comes on early, as a rule 
is first noisy and excited, then becomes milder and muttering and 



THE ^OX-NEURONIC DISEASES 803 

finally sinks into stupor and late coma. Sometimes it alternates with 
a drowsy or somnolent condition. The patient is dazed in it, it mani- 
fests itself in his sleep and with it there are evidences of distinct blunt- 
ing of his sensorium. It usually accompanies the headache and when 
once developed is more or less persistent until the advent of the coma. 

Hyperesthesia of the skin and of all the sensory nerves, particu- 
larly the optic and auditory, is very often a pronounced symptom. The 
patient will complain of the touch of the bed-clothing, of a slight 
draft of air, of the light in the room and of every trivial noise. If 
stupid he will suddenly start when touched. In quite deep stupor I 
have seen the patient move when touched, in a slow, reflex, automatic 
way that was most weird and uncanny. The muscles are also hyper- 
sensitive so that a slight tap will set up a most vigorous reflex. The 
so-called spinal phenomenon, which is a sort of temporary opisthotonos, 
is partly due to muscular hyperexcitability. A light tap on the lum- 
bar muscles sets up a spastic retraction of the column. Sometimes 
the muscles are permanently rigid and spastic. This is particularly 
the case in the neck. The child seems to have its head drawn back- 
ward in an effort to burrow it into the pillow. Disease in the pos- 
terior fossa especially provokes this symptom. 

Another expression of the general muscular rigidity is seen in 
Kernig's sign. At one time this was supposed to be pathognomonic 
of meningitis. It has been seen, however, in many other diseases, 
though it is a valuable one in meningitis. It is easily tested. With 
the patient sitting or lying on his back, place the thighs at right angles 
to the body and note how impossible it is to completely extend the 
legs upon the thighs. The sign may be unilateral, as I have several 
times seen it, or bilateral as it usually is. The rigidity and retraction 
of the abdomen gives it the well known scaphoid, or boat-like appear- 
ance. 

All of the nerves of the body, especially the cranial nerves, may 
enter into the make-up of the clinical picture. Irritability, rigidity and 
paralysis may be among their exhibitions. A certain amount of local- 
ization of the lesion can be determined by the general and cranial nerve 
symptoms. The latter, for instance, are more obvious in basal men- 
ingitis ; hemiplegic and monoplegic phenomena in vertex meningitis. 
Even unilateral hyperesthesia and hemianesthesia have been seen. 

Pupillary changes are very frequent and important signs of the 
disease. As a rule the pupils are bilaterally, very rarely unilaterally, 
contracted in the earlier stages of the affection ; dilated in the later. 
Ptosis and strabismus, and even nystagmus, are present at times and 
easily accounted for. Strabismus is particularly important, especially 
if it shows a tendency to be transient at first or present only on move- 
ment. 

Implication of the facial nerve occurs often. The facial mus- 
cles are spasmodic at first, then rigid and later on partially paralyzed. 
Trismus may be present. The paralysis is of the lower motor or peri- 
pheral type with partial reaction of degeneration. Other motor cranial 
nerves may be included as shown by the difficulty of mastication, of 
swallowing, of articulation, of vocalization, and of glossal movement. 



804 THE NON-NEURONIC DISEASES 

The vision is sometimes partially affected. Optic neuritis, and 
even atrophy is not uncommon in basal meningitis, but it is far less 
frequent in the purulent meningitis of the vertex, it is very rarely 
complete enough to eventuate in a choked disc, and as a result the 
vision is but little decreased. 

The reflexes, trophic and vasomotor symptoms are not particu- 
larly significant. The deep reflexes during the irritative stage are in- 
creased but as stupor comes on they diminish. Among the vasomotor 
manifestations is the well-known tdche cerebrate, of the French authors. 
Drawing the thumb nail across the skin, a brilliant and more or less 
permanent red line is produced. This phenomenon is seen in so many 
other diseases that it has no special value. In many long running cases 
there is a strong tendency to the formation of bedsores, vesicles, etc. 
Hence hot bottles and other irritants must be used cautiously. 

Early in the disease general convulsions or even unilateral con- 
vulsions may occur but they are not common. 

Diagnosis. — The diagnosis of acute leptomeningitis is not dif- 
ficult if the case is a typical one and not obscured by the presence of 
another more general infectious process. Mistakes are constantly 
made, however, as the disease is rarely typical, as it is very often asso- 
ciated with an over-clouding septic process elsewhere, and as prac- 
titioners too often lay too much stress upon special symptoms. 

In recognizing the disease its etiology is a matter of very great 
importance. Not only the disease itself is rendered probable but the 
nature of the inflammation and the location are to be quite positively 
inferred from the existence of a general infection, like pneumonia 
and septicaemia or of a neighboring nidus of suppuration like chronic 
otitis or trauma. 

The onset and character of the symptoms should be carefully 
noted. They appear somewhat abruptly or rather acutely as signs of 
an infective process: chill, fever, vomiting, headache, rapid pulse, irreg- 
ular respiration, constipation, febrile urine. Soon the signs of cere- 
bral irritation or compression appear: persistent headache, delirium, 
convulsions, stupor, retraction of the neck, contraction followed by 
dilatation of the pupils, high temperature with slow pulse and irregu- 
lar breathing, Kernig's sign, and disturbed vision. Finally focal signs 
and terminal coma make the case plain. 

This picture may vary in details but in the main it is so charac- 
teristic that the presence of meningitis can hardly be overlooked. The 
greatest danger is that of calling many diseased states and many 
other affections with a symptomatology which resembles in some of 
its features the symptomatology of meningitis, the latter disease. Vor 
this reason the term meningitis appears much more frequently in clin- 
ical than in autopsy records. There is not a symptom of meningitis 
that does not belong also to some other disease prominently, and many 
combinations of the. symptoms are to be seen in other conditions. All 
of which again emphasizes the fact that the diagnosis of acute menin- 
gitis must be made upon the symptomatic presentation of the ease in 
toto, and that its differential diagnosis from other troubles must be 
attained both by direct and indirect or exclusion methods. 



THE NON-NEURONIC DISEASES 805 

Perhaps the commonest mistake that is made is to diagnose an 
incipient infectious fever of atypical onset for meningitis. This error 
is more frequent than the reverse, namely, the diagnosing of a men- 
ingitis as a simple infectious fever. Typhoid and pneumonia probably 
are the leading culprits in this respect, though septicaemia, pyaemia or 
any of the other septic affections may cause the error. If the lungs are 
affected their examination, as well as the presence of all the usual 
signs of a pneumonitis, will indicate the nature of the malady. Adults, 
and especially children, have headache, delirium, vomiting, fever and 
stupor as a part of the general infective process without meningitis, 
hence the latter must not be inferred from these symptoms alone. 
Focal symptoms, signs of cerebral irritation, pupillary irregularities, 
twitchings, convulsive movements, optic neuritis, progressive advance- 
ment of all these manifestations from a mere initial transiency to a 
more or less permanency, are the aids in determining a meningitis. 
If the trouble be typhoid fever the rose spots, the characteristic stools, 
the course of the temperature, the enlargement of the spleen and the 
Widal blood test will be present ; if meningitis, the general and focal 
signs of this trouble will be in evidence. Jenner pointed out long ago 
that simple febrile headache ceases with the onset of delirium, whereas 
in meningitis it continues with the delirium and even with the stupor. 
Septicaemia is to be suspected from the absence of the more charac- 
teristic clinical picture of meningitis, and the presence of repeated 
chills, cutaneous and retinal hemorrhages, swelling of the joints and 
suppurative processes generally. 

A history of ear disease and the examination of the ear and mas- 
toid cells will help to distinguish a cerebral abscess in the posterior 
fossa from a meningitis in the same locality. This distinction is 
always difficult, however, particularly as some leptomeningitis may 
accompany even an extradural abscess. Much more difficult to com- 
prehend are those cases of purulent otitis with cerebral manifestations 
much like those of a meningitis, which rapidly get well after opera- 
tion, followed by drainage of the ear and mastoid bone. A pyaemia 
may explain some of the symptoms but the occasional optic neuritis, 
strabismus, aphasia and other focal symptoms cannot be so accounted 
for ; and the recovery is too rapid and complete to suspect the presence 
of a meningeal inflammation. 

Retraction of the head is seen in rheumatism of the muscles of the 
back of the neck but the other characteristic signs of meningitis, espe- 
cially the involvement of the cranial nerves, are wanting. 

Urcemic poisoning ofttimes resembles an irritative meningitis. 
Unlike the latter disease the urine contains casts with the albumin, and 
the focal symptoms are wanting. 

Simple meningeal hemorrhage is abrupt in onset, apoplectic in 
character and without the febrile and septic manifestations. 

Intracranial tumor produces headache, vertigo, stupor, but not 
the septic and febrile symptoms. Choked disc and even optic neuritis 
are comparatively rare in meningitis. 

An acute syphilitic meningitis may be determined by the history 
of the infection and the results of antispecific medication. 



8o6 



THE NON-NEURON IC DISEASES 



Pseudo-meningitis is a complexus of symptoms which resembles 
that of a true meningitis but which upon autopsy reveals no indica- 
tion of the latter. Congestion, oedema and other changes have been 
noted. Quincke's hydrocephalus, alcoholic, so-called, serous menin- 
gitis or "wet brain," and some other forms of developmental and 
toxsemic anomalies belong here. It is possible that mild auto-intoxi- 
cation from gastrointestinal catarrh sometimes causes these pseudo- 
meningitic symptoms in children. In all of these cases whether hydro- 
cephaloid, encephaloid, toxaemic or congestive, the absence of the char- 
acteristic febrile phenomena, the peculiar history of the cases, the non- 
purulent indication of the entire trouble, the absence of the focal symp- 
toms and the non-meningeal traits of the disease in its general course 
are to be made note of. 

Some very awkward errors have been committed between hysteria 
and meningitis. Oppenheim was called to see a woman who had had 
her head shaved and antimonial ointment rubbed on it, and yet who 
was out of bed, well and attending to her duties in a few hours. This 
mistake is more likely to occur between hysteria and tuberculous men- 
ingitis. A full appreciation of the real nature of hysteria, a psychosis, 
and the detection of distinct organic symptoms, such as the fever, the 
pupillary changes, the optic neuritis, the incontinence of urine, the 
cutaneous trophic lesions, will help to distinguish one disease from 
the other. The psychic excitement, the psychic distribution of the 
sensory phenomena and paralyses, the variability, and rapid change- 
ability of these under psychic influence are unmistakable in hysteria. 
The permanency of psychosis or psychic traits in the clinical picture 
indicate the organic disease. Errors are liable either way, hysteria 
for meningitis or meningitis for hysteria. 

During the last few years lumbar puncture has been employed to 
a considerable extent, in diagnosing meningitis. Beyond indicating the 
presence of certain inflammatory ingredients in the cerebrospinal fluid, 
and thereby demonstrating the presence of inflammation somewhere in 
the cerebrospinal canal, it cannot be said to have proved itself a ver\ 
definite diagnostic procedure. The risks attending it so far outbalance 
the smallness and uncertainty of the knowledge obtained by it, that it 
cannot be recommended as a routine method. In certain cases where 
the diagnosis is absolutely impossible by the symptoms, and it is im- 
perative that the nature of the disease should be definitely known, it 
may be resorted to. The details in regard to it will be found discussed 
in an earlier section upon diagnosis of diseases of the nervous sys- 
tem or of the spinal cord. The cerebrospinal fluid is to be examined 
physically, chemically, microscopically and bacteriologically. The find- 
ings will be uncertain and on account of adhesions here and there 
between the inflamed membranes, shutting off parts of the central 
cavity, nothing definite will be learned as to the location of the inflam- 
matory process. The chief information obtainable from the proeedure 
is in regard to the bacteria when they are reeovered from the fluid. 
and the presence of an actual inflammatory lesion. There are no - 
cial physical changes except perhaps a slight thickening and clouding 
of the fluid in some of the cases. The presence of large numbers oi 



THE NON-NEURONIC DISEASES 8o # 7 

leucocytes will indicate a purulent meningitis. The bacteria that may 
be isolated are especially the streptococcus, the staphylococcus, the 
pneumococcus, the meningococcus intracellular is, the diplococcus 
lanceolatus and the tubercle bacillus. The albumin may be increased 
and some blood may be present. 

Prognosis. — This is generally bad. Recovery from purulent 
meningitis never occurs. Some simple forms have become chronic, 
while a few have recovered. Gowers, however, cites two recoveries 
from the symptoms of meningitis in post-puerperal septicaemia. The 
difficulty of the diagnosis always casts a doubt upon the reported re- 
coveries and yet warns us never to be too positive in holding out an 
unfavorable prognosis. 

Coma is practically a fatal sign. The less acute the disease is 
the better the chance of its becoming chronic or disappearing entirely. 
If coma does not come on for three or four weeks, the chance of es- 
caping death is that much improved. Traumatic cases and those sim- 
ple cases due to adjacent disease are perhaps the least grave. Sinus 
thrombosis and cerebral abscess are not uncommon complications and 
enter somewhat into the character of the prognosis. 

Treatment. — In a disease so invariably fatal one approaches the 
question of treatment with a degree of hesitancy. Certain measures 
and certain remedies have been recommended, and prophylaxis is 
always in order ; but after all has been done, it will be found that the 
course of the affection has been but little modified. 

The primary disease or source of infection should always be 
attended to, of course. An otitis media, a diseased mastoid, a puru- 
lent rhinitis, any abscess or suppurative focus in or near the cranium, 
should receive proper surgical treatment. An incipient meningitis may 
be checked thus. Cranial traumata should be properly dressed and 
trephining should be thought of in meningo-encephalitis. 

The patient should be put absolutely at rest in bed and all noise 
and light excluded from the room. The ventilation should be free ; 
the diet should be light, nutritious and frequently given. If swallow- 
ing is difficult, nutrient enemata may be resorted to. The temperature 
is to be kept within bounds by cool sponging, and the pains are to 
be assuaged by opiates, phenacetine and antipyretics. The bowels 
should be opened freely with calomel and salines. Diuretics are als > 
commendable. 

The rationale of bloodletting, counter-irritation, cold douching 
of the head for a suppurative process is not very apparent. These 
measures all have their advocates, however. Their employment en- 
tertains the attendants more than it benefits the patient. 

In robust subjects and where the disease has followed a sunstroke. 
mental shock, trauma or other cause of congestion, a few leeches may 
be applied to the mastoid region. Not much blood ought to be ab- 
stracted, however. Most of these patients are already thin and anaemic 
and can ill afford to lose any more blood. Cold may be applied to the 
head with advantage. The headache is sometimes relieved and the 
temperature noticeably lowered. The cold (louche, the ice bag, the 
coiled tubing made to fit the head like a cap and to carry a stream of 



808 THE NON-NEURONIC DISEASES 

cold water continuously, or cracked ice in a towel, may be used for 
this purpose. Counter-irritation with antimonial ointment after shav- 
ing the head, the application of vesicants to it, the use of fly-blisters 
or mustard to the neck and similar measures have been all recom- 
mended but are illogical, discomforting to the patient and without the 
slightest ultimate benefit. If it is thought best to counter-irritate, a 
few light touches with the Paquelin cautery is the best way to do it. 
While this is being done, hot applications should be applied to the 
lower extremities. A treatment strongly commended abroad is the 
rubbing of the head with a twenty per cent, iodoform ointment. 

Internally iodide of potassium, mercury, perchloride of iron in 
large doses, iodoform, gr. vj to gr. xij, daily, have all their advocates 
and are always available for trial. The vomiting is controlled usually 
by dietary measures, absolute quiet and the swallowing of pieces of 
cracked ice. It is a cerebral vomit, however, and is therefore abso- 
lutely uncontrollable until the cerebral excitement subsides somewhat. 
Digitalis may be given to support a weak pulse. Salicin and quinine, 
sometimes given for the elevated temperature, do not seem on that 
account to ward off in the least the fatal issue. 

Surgery has been appealed to in this disease with some slight de- 
gree of success apparently. Ventricular puncture, incision of the dura 
and evacuation of the exudate in the meninges has seemed to effect 
some recoveries. Lumbar puncture also has been successfully em- 
ployed by Quincke, Furbringer, Lichtheim and others. The spinal 
column has been trephined, the dura incised, and drainage established. 
In spite of the few apparent successes by these various measures, they 
are in need of further trial before a final opinion can be passed as to 
their actual value in the long run of cases. 

Epidemic Cerebrospinal Meningitis. — This is sometimes called 
Spotted Fever, occurs both epidemically and sporadically, and is due 
to a special microorganism. An acute purulent leptomeningitis is its 
most prominent lesion and the cause of its leading symptoms. Epi- 
demics have occurred in nearly all the countries of Europe and in the 
United States, causing great destruction of life. Four thousand peo- 
ple died of it in Sweden alone between the years of 1854 and i860. 
Severe outbreaks took place in the United States from 1805 to ^o. 
in France between 1837 and 1850, in other parts of Europe between 
1854 and 1874, and in a great many regions since 1875. Maryland was 
visited by it in 1892, New York in 1893, Boston in 1898. Since the 
first description of it by Vieusseux during the outbreak in Geneva in 
1805, the disease has been closely studied by Danielson and Mann. 
Jackson, Welch, Warren, North, Stille, Hirsch, Councilman, Mallory, 
Wright and others. Wright's contributions to the literature of the 
subject are especially valuable. 

Etiology. — The essential cause of the malady is a specific germ 
but there are certain other moments that enter into its etiology and 
must be taken into account. Children constitute the majority of its 
victims, though it may occur at any age. In civil life children and 
young adults manifest a particular susceptibility. Of course, adults 
make up the list of cases when it occurs in military life. In some 



THE NON-NEURONIC DISEASES 809 

epidemics adults have escaped entirely. Males outnumber females 
somewhat. Cold and temperate climates constitute its favored locali- 
ties, and the Spring and Winter its choice seasons. Endemic influ- 
ences are practically nil, as the disease is seen to break out in widely 
separated and most dissimilar iocahties. It does not seem to be directly 
contagious nor invited by personal habits or characteristics. Unsani- 
tary surroundings, crowding together, as in tenement houses or mili- 
tary barracks, the squalor and wretchedness of the cities, seem to 
foster it. Babes nursing sick mothers have escaped; attendants upon 
the sick are rarely attacked; and the handling of the clothing and 
excretions of the sufferers does not seem to be particularly danger- 
ous. Over-exertion, all conditions of bodily and mental depression, 
association with pigs and dogs afflicted with a similar affection, as 
noted in some of the Irish epidemics, predispose to it. Immunity is 
not conferred against a second attack. Country districts are not ex- 
empt, and the disease very often returns in the same locality. 

Pathology and Pathogenesis. — As a rule the intracranial find- 
ings are about the same as those described under the previous section 
headed acute purulent meningitis. The pia-arachnoid is soft, red, con- 
gested, opaque and filled with a creamy, purulent exudate over the 
entire brain, but especially at the base. The convolutions of the hem- 
ispheres, the basal structures and the roots of the cranial nerves are 
bathed in the pus and hugged by the intensely congested membrane. 
By the fibrino-purulent exudate the meninges are thickened not only 
at the base of the brain and vertex but up and down the posterior sur- 
face of the cord also, especially in the dorsal and lumbar regions. In 
the more chronic cases patches of scattered yellow indicate the earlier 
presence of the exudate. The ventricles are dilated, sometimes to an 
enormous extent. Pus appears in them as well as in the posterior 
horns of the cord. The neighboring brain substance is softened and 
damaged, compressed by the thickened meninges on one side and the 
dilated ventricles on the other, and reveals foci of old hemorrhagic 
extravasation and even of sharp meningo-encephalitis. Small abscesses 
may be present also. All of the cranial nerves, but especially the optic, 
the trigeminus, the facial and the auditory, and all of the spinal nerves, 
may be found imbedded in and infiltrated by the exudate. The 
labyrinth as a consequence may become involved. Otitis media with 
perforation, irido-choroiditis and panophthalmitis may all follow. In 
other parts of the body signs of bronchopneumonia, pleuritis, enlarge- 
ment of the spleen, acute nephritis, swelling of the intestinal follicles 
and disease of the joints may be observed. 

In some cases death takes place so swiftly that none of these con- 
ditions have had time to make their appearance, and therefore, there 
are no post mortem findings. In light cases sometimes only congestion 
of the meninges and a mere trace of an exudate are to be discovered. 
There is much variation in this respect and so wide are the differ- 
ences that the disease has actually been classified in types, such as the 
malignant, the mild and the aborted, the acute, intermittent and chronic. 

A microscopic and bacteriological examination of the exudate has 
lately given us most valuable information as to the probable cause of 



8lO THE NON-NEURONIC DISEASES 

the disease. Polynuclear leucocytes are found closely packed in the 
fibrinous material, also cells two to eight times the diameter 
of a leucocyte. In variable number many diplococci also are found, the 
most frequent one being - the diplococcus intracellular is meningitidis, 
described by Weichselbaum in 1887. The polynuclear leucocytes are 
almost constantly the habitat of this microorganism. Many believe 
that is the cause of spotted fever because it is so constantly observed. 
Other microorganisms that provoke or at least one associated with 
acute purulent meningitis have also not infrequently been seen, so that 
some pathologists still maintain that we are not yet in a position to 
affirm positively that the diplococcus intracellularis is the cause of 
cerebrospinal fever. It is not like Fraenkel's pneumococcus, though 
the latter has often been associated with it in this and other forms of 
acute meningitis. In tuberculous meningitis, and even in the nasal 
mucous membrane of perfectly healthy children, the Weichselbaum 
diplococcus has been observed. 

Further study of the bacteriology of this form of meningitis would 
seem to be desirable therefore before its pathogenesis can be dogma- 
tized upon. 

Symptoms. — As the clinical picture is such a varied one it will 
be well perhaps to describe a typical case and discuss its main symp- 
toms in detail first, and then enumerate and point out the differences in 
the recognized types afterwards. 

There are two great groups of clinical signs of the disease in 
every case. The first are those of the general profound toxcemia and 
constitutional malady; the second are those that belong to the menin- 
geal inflammation and some complicating features. 

The period of incubation of the germ is unknown and the prod- 
romata are not usually very prominent. Most cases begin abruptly or 
if there are premonitory indications, they consist of the usual feeling 
of malaise, slight headache, backache, dullness, nausea, constipation 
and anorexia. Much more commonly there is a chill, a sudden access 
of fever, vomiting and a severe headache. The scene opens just as 
nearly all of the infectious fevers do. Vertigo, restlessness, insomnia. 
and general convulsions may be added to it. In a day or so the men- 
ingitic symptoms begin to declare themselves. The headache increases 
and becomes intense, especially in the occipital region and down the 
back of the neck. The temperature steadily rises to 100 degrees or 102 
degrees, and the pulse becomes rapid and irregular. Both run a varied 
and irregular course. With the pain in the back of the neck, the mus- 
cles become rigid ana there is marked nucha! retraction. This has 
been so extreme that the head hung back between the shoulder blades. 
The spine gradually becomes arched so that there is opisthotonos. 
Orthotonos is probably more frequent than opisthotonos. Pains and 
rigidity, severe in type, appear in the limbs. Every touch to the 
patient, every effort to move him causes him to cry out with the 
agony. He writhes, his face becomes contracted and he shows in an 
unmistakable manner that he is in extreme pain. Trismus, abdominal 
retraction, strabismus and a general muscular rigidity so that the pa- 
tient can be lifted like a statue, are all present. The maxillary, spinal 



THE NON-NEURONIC DISEASES 8ll 

truncal and leg and arm muscles are all involved and reveal, with the 
tenderness and shooting pains, without ever passing into paralysis, the 
.typical picture of cerebral and spinal meningitis with implication of 
the cranial and spinal nerve roots. The sensorium for a time is clear 
but soon delirium and a clouding of the faculties add themselves to 
- the complexus of manifestations. The cephalalgia continues, the fever 
exacerbates and a wild and maniacal delirium seizes the patient. He 
raves and strikes out and becomes a perfect fury. The delirium is a 
gradual and early manifestation. In the beginning, it is associated 
with violent erotic Or sexual excitement. In a few days it exhausts 
itself and sinks rapidly into the stupor and comatose condition. Just 
before death, which occurs in these cases in from ten days to a couple 
of weeks, the fever, which has been very erratic, suddenly rises to 106 
degrees or 108 degrees, the pulse becomes small, feeble and irregular, 
the respirations grow labored and assume the Cheyne- Stokes type or 
sighing characteristic, and the coma becomes profound and complete. 
Among the other symptoms are to be noted the coated tongue, 
foul breath and constipation. There is retention and incontinence of 
urine. Some albuminuria is present ; sometimes glycosuria. The 
urine at first is typically a febrile urine but later it is apt to be exces- 
sive in amount. The spleen is almost constantly enlarged, though on 
account of the pain cannot generally be palpated. 

Later manifestations are of a paralytic and trophic character. The 
name of the disease, spotted fever, is given on account of the marked 
cutaneous symptoms. They are not a constant feature of the disease, 
however. The skin may be merely erythematous or mottled. Rose 
spots, as in typhoid fever, sometimes are present ; at other times only 
petechias and scattered purple spots are to be seen. Herpes occurs 
more frequently than it does in pneumonia or intermittent fever. Other 
•cutaneous manifestations that have been noted are erythema nodosum, 
■ecthyma, urticaria and pemphigus. Gangrene of the skin has been a 
r are observation. Other complications of the meningitis are conjunc- 
tivitis, a neuroparalytic keratitis, chemosis, mydriasis, optic neuritis, 
strabismus, facial paresis and deafness. The implication of the cra- 
nial nerves, of course, explains these symptoms. Purulent irido- 
choroiditis is a particularly frequent trouble, and is in all probability 
the result of metastasis. Amaurosis is its ultimate result. Aphasia has 
"been seen. 

General convulsions are not common except in children. Hemi- 
plegia and monoplegia may be present but hidden by the clouded con- 
sciousness. Paraplegia, loss of patella reflex ( increased usually at 
first), paralysis of the sphincter vesicae and girdle pains indicate the 
disease process in the cord. Bedsores, joint troubles and extreme 
emaciation occur in the protracted cases. 

As these symptoms are not always the same in all cases, as not 
all cases are fatal by any means, and as the disease runs a course any- 
where from a few hours to several months, clinicians have established 
the following types : 

I. The Malignant or Fulminant Form. — This may appear epi- 
demically or sporadically. The disease seems to burst out all at once. 



8l2 THE NON-NEURONIC DISEASES 

The chills, headache, fever, vomiting, delirium, somnolence, convul- 
sions, spasms, rigidity and terminal coma appear suddenly and run 
their course in a few hours. The onset, the development and the termi- 
nation are swift and terrible. In one case the whole gamut of symp- 
toms from start to finish was run in five hours. Other cases have died 
in twenty-four hours or less. Truly may these cases be styled apo- 
plectic. 

2. The Ordinary Form. — This has been described. 

3. The Rudimentary or Abortive Form. — These cases are very 
confusing when they occur sporadically, though during an epidemic 
they may be correctly recognized. The symptoms are all mild and in- 
definite. The headache and backache are slight. Possibly there is some 
restlessness, irritability, insomnia or dullness. There may be nausea. 
The nuchal muscles may seem a little stiff. Fever is slight or absents 
Two classes of these cases are recognized. In one the symptoms be- 
gin abruptly and with considerable severity, but in a few days they 
die out or subside to almost nothing. In the other they are never more 
than slight and the cases are entirely ambulatory. 

4. Intermittent Form. — These are protracted cases, often run- 
ning many months with complete intermissions or marked remissions 
in all of their symptoms. They may even appear as quotidian, tertian 
and other types. Some cases run a steady, severe course at first, and 
then pass into convalescence as an intermittent disease. Pyaemia rather 
than malaria is the suggestive feature about the fever. 

5. Chronic Form. — This is frequent according to Heubner. 
With a very variable symptomatology, these cases run along, now up,, 
now down, but never intermittent, for three and six months. Intense 
marasmus usually supervenes. As Osier says, it is not improbable that 
hydrocephalus or intracranial abscess is at the bottom of these. 

Diagnosis. — The diagnosis of epidemic cerebrospinal meningitis 
offers the greatest difficulties only when the case is a sporadic one, or 
in those cases that now and then continue- to break out in a locality 
where the epidemic has prevailed. If the complete picture of the dis- 
ease is kept well in mind, the general septic febrile process, the charac- 
teristic cerebral and spinal meningitic manifestations, the marked 
cutaneous exhibitions and the frequent complications, such as pleurisy, 
broncho-pneumonia, pericarditis, parotitis and implication of the artic- 
ular joints, I think one will have little trouble in making a diagnosis, 
even though all of these indications are not present at the same time. 
The history of the case must be always given due weight. Perchance 
the patient has had the disease before, or there has been a recent epi- 
demic in the vicinity. If the epidemic is raging at the time, there is. 
no doubt about the diagnosis whatever. 

Sporadic cases are hard to distinguish sometimes, especially when 
protracted and not very violent, from tuberculous meningitis. Tuber- 
culosis elsewhere or in the family is suggestive of the latter. More- 
over the spinal symptoms are not so prominent, whereas the mental are 
slightly more so in the tuberculous disease of the membranes. The 
herpes and other skin, manifestations, the enlarged spleen, the com- 
plications, speak for the epidemic disease, or at least they are not the 



THE NON-NEURONIC DISEASES 813 

same as they are in tuberculous infection. Lumbar puncture and the 
finding of the specific micrococci or bacilli offers the crucial test of 
.the true nature of the trouble. 

Atypical forms of typhoid fever and cerebrospinal meningitis may 
oe confounded with each other. In the former the temperature runs 
.a different course, there are loose stools with tympanites and an ab- 
sence of the herpes, joint troubles and characteristically combined cere- 
bral and spinal meningitis manifestations. Here again lumbar punc- 
ture comes to our rescue. 

Pneumococcus meningitis, which may occur either alone or as 
an accompaniment of pneumonia, is sometimes very like the epidemic 
form. According to Leichtenstern, with the former the contraction of 
the muscles of the neck is often wanting, while in the latter it is inva- 
riably present. The former quickly leads to delirium and coma, whereas 
in the latter the sensorium is clear for a long time or even throughout 
the entire course of the disease. The former is rapidly fatal, the latter 
Is frequently recovered from. In the former, symptoms pointing to 
-a wide extension of the meningeal infection of the brain and cord, in- 
volving the spinal and cranial nerve roots, are less pronounced or even 
absent as compared with the same symptoms in the latter. Lumbar 
puncture may settle the question to a large extent by discovering the 
pneumococcus in the one case or the diplococcus intracellularis in the 
other. 

Epidemic cerebrospinal meningitis has some imitations in small- 
pox, tetanus, uraemic coma, acute articular rheumatism and hysteria. 
A careful consideration of the history, a thorough examination of the 
patient and the recollection of the clinical picture, in to to, of the spe- 
cific meningitis will enable one to avoid error in the differential diag- 
nosis. 

Prognosis. — This is always serious but not necessarily bad. In 
epidemics the mortality ranges from twenty to seventy-five per cent. 
In children it is more fatal than in adults. Early in the epidemics 
severe cases predominate, later on the mild cases are in the majority. 
Very rapid or very protracted cases are not hopeful. Mild cases that 
run a medium course offer the best outlook. They often get well, 
though usually leaving some defect or complication, such as blind- 
ness or deafness, which are apt to be permanent if they show no signs 
of receding in the first three months after the outbreak of the dis- 
ease. Deep coma, repeated convulsions and high fever are bad omens. 
Existing complications such as pneumonia, endocarditis, and pericar- 
ditis add to the gravity of the prognosis. Fulminant cases destroy t In- 
patient in a few hours or a day or two. Ordinary cases run an irregu- 
lar course, as a rule, of two or three weeks. Protracted cases may 
continue for many weeks. Chronic cases may not be free from signs 
of the disease for five or six months. Sequelae are unfortunately com- 
mon. Death is caused by exhaustion, decubitus, marasmus in chronic 
cases; by the intense intoxication with asphyxia and annihilation of all 
the vital processes in the acute and fulminant cases. 

Treatment. — There is no specific remedy for the disease. After 
placing him in the best hygienic environment, the most we can do for 



814 THE NON-NEURONIC DISEASES 

the patient is to sustain his strength, ameliorate his sufferings and com- 
bat some of the symptoms. Opium usually has to be given freely. 
Morphia administered hypodermically is the best. Mercury, iodide of 
potassium, salicylate of sodium, ergot, belladonna, calabar bean, quinine 
in large doses, digitalis, benzoate of sodium, chloral, potassium bromide 
and alcohol are some of the remedies that have been recommended 
for both the disease in general and to meet special indications. The 
long and varied list of them, and the continued high mortality of the 
disease, demonstrate how futile is practically all of our therapy in re- 
lation to it. 

In regard to bloodletting, hydrotherapy, counter-irritation and the 
application of cold to the head and spine, the same principles are ap- 
plicable here that I suggested under the head of acute purulent menin- 
gitis. Hot baths have lately been very favorably recommended, as also- 
has lumbar puncture. 

Plain, nutritious diet, of milk and strong broths especially, must 
be given during the fever. The stomach tube may have to be em- 
ployed if swallowing is difficult. Stimulants are needed regularly in 
most cases. 

The residual symptoms call for no special treatment. 

Tuberculous Meningitis. — This is a form of meningitis that 
generally runs a subacute course, is due to a specific germ and occurs 
mostly in children. It used to be spoken of entirely, and is even still 
sometimes referred to, as acute hydrocephalus, or "water on the 
brain." Basilar meningitis is another of its more popular synonyms. 
Though its study really dates from the observations of Robert Wright, 
of Edinburgh, in 1768, our accurate knowledge of it was laid down 
by Gerhard, of Philadelphia, in 1832 and 1833. It has a few distinctive 
features that warrant its discussion in a section by itself, though in 
the main it is the same in all respects, except etiology, as all the other 
forms of leptomeningitis. 

Etiology. — The essential cause of the disease is the tubercle 
bacillus. This usually enters the circulation from a tuberculous lesion 
somewhere else in the body, lungs, joints, intestines, and so reaches the 
base of the brain where it sets up its specific inflammation. It is thus 
a secondary disease, or infection. There are cases in which both 
during life and after death no primary focus can be discovered. It is 
always highly probable that the latter has been overlooked for a com- 
plete examination grossly and minutely of all the tissues of the body is a 
very difficult task. Nevertheless it may be true, as believed by some 
authorities, that in a few instances the disease may be primary in the 
brain, the bacilli entering the cranium by way of the nose and cribri- 
form plate of the ethmoid bone. 

A certain amount of predisposition towards the disease is shown 
in the fact that it attacks preferably individuals of a certain age. It 
is frequent in children, rare in adults. It is scarcely ever seen during 
the first year of life. Most cases occur between two and ten years of 
age. The majority of those that I have seen, have been about four 
and six years of age. It occasionally breaks out in early adult years. 
It is exceedingly infrequent after forty. Every explanation hitherto 






THE NON-NEURONIC DISEASES 51 5 

offered to account for the predominance of the disease in childhood is 
entirely hypothetical. Some think it is due to the relative rapidity of the 
vital processes in the growing brain of the child ; others hold that it 
has relationship to the frequency of alimentary tuberculosis in children. 
It has frequently been charged to the ingestion of tubercle-infected 
milk. The eruptive fevers, especially measles, have in a considerable 
number of my cases immediately preceded its revelation. These may act 
along with such assigned subsidiary causes, as cranial traumata, ex- 
cessive emotional excitement, mental strain and alcoholism in dimin- 
ishing the individual's general power of resistence. The bronchial trou- 
bles of measles and pertussis may open the gateway for the infected 
air to scatter the germs into the circulation. Males suffer more than 
females. 

Pathology and Pathogenesis. — The disease may appear any- 
where in the meninges of the brain and spinal cord. In fact many 
of the cases are cerebrospinal meningitis with the cerebral manifes- 
tations masking the spinal. The favorite seat of the trouble seems to be 
the base of the brain, hence the name basilar meningitis. In the vicin- 
ity of the great vessels found here, the arteries branching off from the 
anterior middle and posterior cerebrals, the pia is inflamed, granular 
and covered with an exudate. Around the optic chiasm, in the inter- 
peduncular space, up along the Sylvian fossae, beneath the medulla 
oblongata and cerebellum, and even in some cases up on the convexity 
of the hemispheres and down along the spinal cord, the meninges are 
thickened, opaque and covered with the gelatinous effusion. There 
turbidity, matting together and nodular contents are unmistakable. 
All along the vessels, especially at the points of their bifurcation, or 
branching, are found the miliary tubercles which caused Guersant in 
1827 to use the name granular meningitis. Sometimes these coalesce 
and form larger tuberculous nodules. In these are found the specific 
bacilli of tuberculosis. By stripping off the membrane and holding it 
up before a bright light the tubercles become very evident. They are 
seen to be imbedded in the exudate and also where there are no signs 
of inflammation. They are identical in structure with the same sort of 
tubercles found elsewhere in the body. They may be very numerous or 
only few and widely scattered. The dura may be invaded by them, 
especially in the region of the middle meningeal artery. They are 
sometimes seen in the tunica intima of the arteries in conjunction with 
an endarteritis and a proliferation of the adventitia. In such cases 
the calibre of the vessel may be diminished and a thrombosis occur. 
The choroid plexus is usually included in the infection, and the nodules, 
with redness and the exudate, are seen scattered along the sheaths 
of the cranial nerves. The neighboring brain substance is always more 
or less implicated so that the condition partakes of the nature of a 
meningo-encephalitis. It is injected, infiltrated with leucocytes, oedenia- 
tous, softened in spots and punctated with small hemorrhagic foci. 
Spots of softening from tuberculous arteritis also appear in the basal 
ganglia, cerebral peduncles and the spinal cord, even in some case- as 
far as the filum terminale. The ventricles are usually dilated and full 
of turbid fluid, producing a condition of internal hydrocephalus. The 



8l6 THE NON-NEURON JC DISEASES 

ependyma is softened and diseased. The fornix and septum lucidum 
are often broken down. As is usually the case in hydrocephalus with 
ventricular pressure the cerebral convolutions are compressed and 
flattened and the sulci are partially or completely obliterated. Such 
is the pathological picture of an ordinary case of tuberculous menin- 
gitis. There are cases, however, which are swift and fulminant in 
which not much more than the presence of the tubercles and intense 
congestion can be discovered. In other cases the disease runs such a 
prolonged course that a superficial, strata-like exudate with spots of 
caseation and other evidences of old or chronic inflammation are all 
that is to be seen. 

Symptoms. — Clinically tuberculous meningitis assumes a varied 
guise. It is an infectious disease usually with more or less prominent 
symptoms of local lesions in other parts of the body as well as in the 
brain. On this account we usually find the trouble in weak, puny, pale, 
anaemic, ailing and badly-nourished individuals, who at the same time 
have a diseased lung, joint, ear or lymph glands. The general debili- 
tated physique and its functional inadequacies present their own par- 
ticular symptomatology. The local nidus of the disease adds its quota 
to the tout ensemble of the clinical picture. In the midst of all this 
the clinical signs of the meningitis must be traced out ere a diagno- 
sis of the latter can be assumed. To add still more to the difficulty, 
the meningitis itself may be a very diffuse or limited lesion, involv- 
ing large or small areas of functional brain substance ; it may be a 
rapid and stormy process, or a quiet, progressive inflammation, each 
with its own variety of symptoms ; and finally it may im- 
plicate such functionally dissimilar elements, in such a variable 
way that nothing definite can seem to be made out of the 
complex, clinical presentation. In' view of all these difficulties it is 
not surprising that the trouble is so often overlooked or not recog- 
nized until coma and death are close at hand. The natural hesitancy, 
born of a desire to avoid, if possible, the final confirmation of so sad 
and fatal an affliction, clouds the physician's best judgment even when 
it is struggling in the midst of one pf the most difficult diagnostic prob- 
lems that medicine sometimes offers. 

One should approach the diagnosis of tuberculous meningitis 
therefore carefully, with a clear and unbiased reasoning faculty, and 
with a perfect mental conception of what a typical case should look- 
like. For there is a clinical picture of tuberculous meningitis that is 
sufficiently distinct and uniform to warrant its being described as a 
disease per se, however surrounded or clouded it may be by other man- 
ifestations. So clear and distinct is this portraiture that many divide it 
into three periods, the prodromal, the irritative and the paralytic, and 
give a special description of each of them. 

Premonitions of tuberculous meningitis may occur weeks and 
months before it frankly announces its presence. They are sometimes 
very marked and in none but a tyro would fail to awaken a strong sus- 
picion. At other times they are so slight and evanescent that their 
significance is hardly appreciable until the disease is sufficiently ad- 
vanced to make a diagnosis a comparatively easy matter. The child's 



THE NON-NEURONIC DISEASES 817 

disposition indicates a change. It is somewhat fretful and irritable 
and cross. It seems to be subject to spells and paroxysmal outbreaks 
of crying and worrying. In the intervals it may appear somewhat in- 
different or unsocial and dull. As these changes often follow an 
attack of measles or other disease or are associated with some cachectic 
condition, they are attributed to general ill health. After awhile attacks 
of headache appear at various intervals and the child complains of the 
acuteness and darting character of the pain. In one case the parents 
noted months before an unsteadiness of gait which they attributed to 
convalescent weakness. In sleep the threatened victim is restless, tosses 
about, talks, has terrifying dreams and cries out now and then or sud- 
denly wakens up with a start. As the case advances the headache be- 
comes excruciating and unnerving. Periodical at first, it is now more 
or less persistent with intolerable exacerbations. The little patient 
seizes his head with his two hands and screams with the agony. He 
instinctively avoids the light and the slightest noise rouses him into a 
frenzy. A mild delirium now begins to assert itself and with it an un- 
conquerable insomnia. Unexpected and unaccountable attacks of vom- 
iting take place. The appetite is lost. Constipation is troublesome. 
Emaciation shows itself. Occasionally there will be a slight, irregular 
elevation of the temperature. 

Many cases seem to glide gradually from the prodromal condi- 
tion into the easily recognized state of the disease. In other cases, 
however, perhaps the majority, after a few weeks of these indefinite, 
transient exhibitions of peevishness, headache, fever and vomiting, the 
child suddenly becomes violently ill. There is a chill or a convulsion. 
with violent vomiting, sudden rise of temperature, intense headache 
and many of the signs that accompany the outbreak of all the infec- 
tions fevers. Ofttimes over-exertion at play, exposure to the hot sun, 
or indiscretion in eating seems to precipitate the attack. Unless he is 
suspicious and guarded, the physician will be very liable to ply reme- 
dies to correct the supposed indigestion and offer a favorable prognosis. 
It is a matter of profound chagrin and sorrow to the attendant, as I 
have several times witnessed, when at the end of ten days or a couple 
of weeks coma comes on in spite of all his treatment and hopeful prom- 
ises, and the patient dies while he is forced to admit that if he had 
only been more studious of the case he might have recognized the pre- 
monitory signs many weeks before. 

The temperature rises to 103 degrees. The pulse becomes rapid 
and then slower. The respirations do not change much. The sen- 
sorium remains for a while clear and the headache grows more in- 
tense. A short, sharp, distressing cry, the so-called hydrocephalic cry. 
is vented now and then. The sleep is broken and fretful, or there may 
be insomnia. The muscles begin to twitch and start. The pupils arc 
contracted. Vertigo is complained of. Light and sound are absolutely 
unbearable. Delirium alternates with somnolence. The teeth are 
ground together and the head is burrowed into the pillow. This is the 
so-called stage of irritation. The motor and sensory manifestations 
of it are striking and characteristic. The hyperesthesia, both of the 
general and special senses, is all but too obvious. The patient resents 



8l8 THE NON-NEURONIC DISEASES 

every touch upon his skin and muscular tissues. He doesn't want to 
be moved. He begs simply to be left alone free from contact as much 
as possible of bedding and clothing. Following the early transitory 
twitchings, the muscles of the neck, face, back, arms and legs become 
rigid. Before the contractures become marked the reflexes are notice- 
ably exaggerated and Kernigs sign is pronounced. Trismus is pres- 
ent. The back is bowed in opisthotonos. The abdomen is hard and 
retracted. The arms and legs and hands and feet are all more or less 
flexed, rigid and contractured. In this stage general or partial con- 
vulsions may occur or epileptiform attacks, or brief tetanic contrac- 
tions in the entire musculature of the body. 

Gradually these symptoms lead into the stage when stupor reveals 
the exhausted and hydrocephalic conditions of the encephalon. All 
signs of irritation subside and the patient lies still, dull, apathetic and 
uncomplaining. He may utter an occasional cry or there may be a 
slight convulsive wave pass over the body but as a rule all is still. The 
coma is clearly deepening and the earlier suffering is being replaced 
bv an appearance of death. The pupils are now dilated and unequal. 
Vision is obscured, or at least there is no reflex response as in health. 
The eyeballs are rolled from one side to the other. Strabismus is pres- 
ent ; sometimes a condition not unlike nystagmus. In a little while 
signs of optic neuritis or choked disc may appear at the fundus. Oc- 
casionally a tuberculous choroiditis can be made out. Respirations be- 
come sighing. The temperature fluctuates widely even from day to 
day. The pulse usually drops below the normal. The skin is erythe- 
matous in patches and if rubbed with the finger nail exhibits the un- 
important tdche cerebrate of the French writers. The bowels are still 
obstinately constipated and the abdomen is boat-shaped. 

Gradually from this stage the patient passes into the final or 
paralytic stage in which paralysis, not complete, however, of the cra- 
nial nerves and of special groups of muscles, and coma constitute the 
predominant symptoms. An occasional twitch or convulsion may occur 
and with a great effort the child may be aroused. As a rule, however, 
intense coma, immobility with contracture or relaxation and a general 
collapsed typhoid state is the condition present. After awhile the 
patient cannot be roused at all. Involuntary evacuations of the bowels 
and bladder take place. The pulse becomes rapid and feeble. A low 
delirium may continue. The temperature falls to subnormal, even to 
94 or 93 degrees, rising suddenly to 106 or 108 degrees just before 
death, which occurs usually from two to three weeks after the onset 
of the malady. 

In adults the disease may appear abruptly, run a violent course 
with exaggeration of all the symptoms and terminate in death in a few- 
days. Children also are occasionally attacked this way. Afore often. 
however, in children the disease runs a more protracted, irregular 
course. Even remissions occur that raise false hopes of recovery. In 
these cases monoplegias, hemiplegias, aphasia, Jacksonian epileptiform 
phenomena, rigidity followed by temporary relaxation or permanent 
contractures, tremors, athetoid, cataleptoid and tetanic conditions need 
not surprise one if they appear. A moment's consideration of the 



THE NON-NEURONIC DISEASES 819 

lesion and its location, the thickenings, the arteritis, the hemorrhages, 
thromboses and foci of softening in and about the area supplied by 
the middle cerebral artery will explain them. 

Diagnosis. — In a frank case, the diagnosis of tuberculous menin- 
gitis is not a matter of great difficulty. The discovery of a tuberculous 
focus somewhere else in the body, the prodromal history, the onset, 
course and character of the symptoms present, if carefully analyzed and 
properly valued in their various relationships, will afford an outline 
picture that can easily be recognized. And yet, as I have said before, 
sometimes the diagnosis is a most difficult matter on account of the 
irregularity of the symptomatology of the meningitic trouble, and espe- 
cially on account of the masking of the case by the symptoms of the 
complications that are often present. Lumbar puncture is usually con- 
clusive even though the bacilli are not always recovered. The menin- 
gitic character of the fluid, the evidence of leucocytosis, its ready 
coagulability, its high pressure, its cloudy, purulent appearance though 
it may be clear, are all confirmatory when the symptoms point in the 
least toward tuberculosis. 

The trismus in some cases may cause them to be mistaken for 
tetanus. The history of an injury determines the latter, however. 
Typhoid fever and other infectious diseases, gastrointestinal catarrh, 
anaemia, hemicrania may be confused with the early stages of menin- 
gitis. Care in eliciting the minute history of the case and in the personal 
examination of the patient will forestall error. The same may be 
said of general miliary tuberculosis which may or may not have men- 
ingitis associated with it. Sometimes, when meningitis seems to be 
the only affection present, its tuberculous nature can be suspected when 
the prodromal stage is prolonged and preceded even by weeks and 
months of transient premonitions, when the temperature is moderately 
raised, when its entire course lacks violence and great severity, when 
tuberculous choroiditis can be discovered and when the disease occurs 
in a child. 

Prognosis. — This is decidedly bad. The reported recoveries have 
probably been cases that were erroneously diagnosed, in spite of the 
fact that a few such cases have been put upon record by reliable author- 
ities. I have never seen a recovery in a positive case of the disease. 
Freyhan, according to Oppenheim, had a case recover even after the 
tubercle bacilli had been secured from the cerebrospinal fluid. The 
possible contingencies surrounding such a case are so numerous, that 
in view of the almost constant fatality of the disease, one may be 
cused for retaining a doubt in regard to it. The disease runs a more 
typical course in children than it does in adults. Tt may be latent or 
be quite over-shadowed by the primary trouble for a long time. \> 
a local meningitis of the vertex, it may cause only aphasia, hemiplegia, 
Jacksonian manifestations, merely to become generalized years later. 
Tt is believed that some of the so-called aborted cases are due to lulu r 
cular intoxication of the brain rather than a true meningitis. 

Treatment. — Prophylaxis is important. Tuberculous foci should 
always be removed from other parts of the body, surgically or other- 



320 THE NOX- NEURONIC DISEASES 

wise, if possible. A tuberculous child should be treated on general 
principles with fresh air, good food, nutritious diet, careful nursing, 
cod liver oil, and tonics. 

The administration of large doses of potassium iodide (600 grains 
a day in one case that recovered) and symptomatic treatment bounds 
our therapy in this intractable disease. 

Surgical measures such as ventricular tapping as a palliative, tre- 
phining and subarachnoid drainage and lumbar puncture as radical, 
have been tried with a modicum of success. Afore experience will be 
needed before final judgment can be passed upon the operative treat- 
ment of tuberculous meningitis. 

Chronic Meningitis. — Except as a syphilitic product, chronic 
meningitis, is rare, much more so clinically than pathologically, though 
in general practice it is often diagnosed in headache, after isolation and 
following injuries to the head. It may occur at the vertex. On the 
autopsy table it is more often seen at the base. It plays a role in the 
production of intense hydrocephalus by reason of the adhesions it 
causes and the closure of the interventricular openings. Its symptom- 
atology is usually slight? or nil. The symptoms often attributed to it 
are mostly due to compression, congestion and other disturbances of 
the brain substance, especially the cortex. 

In alcoholic subjects there is a condition that is sometimes spoken 
of as serous meningitis. Inflammation is not present, however. The 
headache, slight delirium, mental failure and tendency to optic neuritis 
are due to congestion merely. Intoxication of the brain elements is 
also probably responsible in part for the symptoms. Multiple neuritis 
and hepatic engorgement often complicate these cases. 

Chronic syphilitic meningitis has been spoken of under the head 
of syphilis of the central nervous system. There are many forms of 
obscure basal meningitis in children as well as in adults, which run 
an irregular course and are probably due to inherited syphilis. 

Chronic ossifying meningitis is a pathological curiosity that has 
been seen in some old cases of persistent headache, epilepsy and in- 
sanity. 

There is a chronic infantile meningitis, the non-tuberculous pos- 
terior meningitis of infants that is of considerable interest. It is some- 
times associated with syphilis and may cause a severe hydrocephalus. 
Its chief symptom is retraction of the head, so that it has even been 
called the "cervical opisthotonos of infants." The posterior fossa of 
the skull is its choice location. Sometimes its onset is sudden ; at 
other times it is gradual. Fever, vomiting, rigidity of the limbs and 
convulsions have all been pointed out in connection with it by Gee and 
Barlow. The retraction of the head may be intermittent. Palsy is 
rare. Sometimes there are strabismus and nystagmus. The head be- 
comes hydrocephalic in size- after a time in some cases. Recovery or 
death may take place in from a month to a year or a year and a half. 
Sometimes weeks before death, the child passes into a state n\ stupor 
or coma. Antisyphilitic treatment should always be given a trial in 
these cases. 



THE XOX-XEUROXIC DISEASES 82 1 



CIRCULATORY DISEASES OF THE BRAIN. 

From clinical as well as experimental observation we know that 
the brain is very susceptible of the slightest change in its circulation. 
Just how this is we are not always able to determine. Its functional 
integrity is clearly dependent upon the quality and quantity of blood 
flowing through it, upon the blood pressure, and upon the velocity of 
the flow. The relative importance of these various factors is still un- 
known to us. In the older pathology mere blood pressure and quan- 
tity of blood constituted a basis whereon were erected elaborate clin- 
ical descriptions and symptomatic differentiations. It is probable that 
in an organ so highly vascularized as the brain is and with such a rich 
anastomosis between all parts of its main circulatory apparatus, the 
changes of pressure and amount of blood would have to be compara- 
tively gross to effect marked changes in the cerebral symptomatology. 
As a sort of reaction to this coarse and largely hypothetical clinico- 
pathology of the past, it is now denied by many that any changes, 
capable of being observed at the bedside, take place in the mere pres- 
sure of the blood or the quantity circulating through the brain. This 
is perhaps an extreme in the opposite direction, though it is a whole- 
some protest to the many fine focal and generalized distinctions that 
used to be made in the symptomatology erected upon the old hypo- 
thetical pathology. 

There are symptomatic manifestations, however, that are clearly 
due to circulatory disturbances. In accounting for these, modern 
pathology lays the greater stress upon the quality of the blood and the 
velocity of its flow in the capillaries. The composition of the blood 
we know is subject to great variations. Its corpuscular richness, its 
chemical and bacteriological ingredients, its endogenous and exogenous 
contents, its gases, its specific gravity and physical state are all finer 
factors in influencing the delicate activities of the cerebral neurones, 
it would seem, than are the mere pressure and quantity of the fluid. 
Moreover the rapidity of flow depending largely upon the tension of 
the vascular walls, and causing a correspondingly swift removal of 
deleterious products of metabolism and conveyance to the nerve cells 
of stimulating, nutritious pabulum would also appear to be a more in- 
fluential factor. These facts are supported by experimental research 
and dovetail better with what we know nowadays of cerebral physiol- 
ogy and pathology than the old theories based upon mere hyperemia 
and anaemia. They are founded upon better proofs than the mere 
post mortem macroscopic appearances of the brain. The latter, it is 
now recognized, are to a large extent due to such post mortem influ- 
ences as the position of the corpse, pressure about the neck, tin* 
examination, etc. 

Ante mortem appearances of the face and skin have too long been 
adopted as arguments for a similar condition in the intracranial tis- 
sues. There is no assurety that they are the same, and some facts even 
intimate that they rarely are. Facial pallor during life and cerebral 
pallor after death, do not by any means prove that the brain was in 



822 THE NON-NEURON IC DISEASES 

like condition while the patient was alive and manifesting the symp- 
toms supposed to de due to them. 

Notwithstanding our symptomatology of cerebral anaemia and 
hyperemia is based upon clinical and experimental observations, fur- 
ther studies are needed to determine just how much is due to each of 
the respective factors that always more or less accompany these circu- 
latory conditions, namely, the quantity of the bipod, its quality, the 
pressure of its column, and the swiftness of its flow, yntil we learn 
more about these, we will still have to treat of the clinical manifesta- 
tions under the two general heads of cerebral anosmia and cerebral- 
hypercemia. 

CEREBRAL ANAEMIA. 

It is perfectly reasonable to suppose that under certain conditions 
the quantity of blood in the brain may be diminished, even consider- 
ably, below the normal. What is the normal for any one particular 
individual and how far below the normal can the quantity of intra- 
cranial blood of that individual be reduced before the brain manifests 
it outwardly? Who can tell? Hence when we outline a symptoma- 
tology for cerebral anaemia, it must not be imagined that we attribute 
the symptoms entirely to the mere want of blood. Other unknown fac- 
tors are undoubtedly at work, such as, for instance, the nutritive pov- 
erty of the blood, its altered composition, the shock caused by the sud- 
den disturbance in its flow and the diminished pressure in some cases in 
the blood-vessels. 

Etiology. — So far as we know, cerebral anaemia is both a local 
and general condition and may be dependent upon both heal and gen- 
eral causes. An embolus, for instance, causes a local anaemia, followed 
by other changes in the brain ; a cachetic state of the constitution may 
be accompanied by deficient and bad blood supply. The anaemia may 
therefore be primary or secondary. The immediate and remote causes 
of the condition are therefore innumerable and I can only mention a 
few by way of illustration. 

Severe hemorrhage in some other part of the body, or even in 
the brain itself, may provoke a symptomatic anaemia. The coma of 
hemorrhagic apoplexy is believed to be due partly to the sudden anaemia 
of the cortex caused by the local loss of blood and certainly in sud- 
den and profound hemorrhages from the lungs, stomach, bowels, 
uterus, syncope and other signs of severe cerebral anaemia are often 
observed. The sudden withdrawal of ascitic fluid, paracentesis of the 
abdomen, precipitate parturition, abrupt disturbance of the heart ac- 
tion from valvular or other form of disease, violent cupping, nervous 
collapse as seen in simple swooning, may suddenly diminish the amount 
of blood flowing to the brain. The same condition as a continuous one 
follows probably the exhaustive febrile diseases, cardiac weak- 
ness, partial obstruction by tumor, aneurism and diseased 
blood vessels, and hydrocephalic conditions. Pressure upon 
or ligature of the carotid produces signs of transient cerebral anaemia. 
Vasomotor spasm and anaemia have been blamed for certain forms 
of migrainous headache and epileptiform phenomena. It is thus seen 



THE NON-NEURONIC DISEASES 823 

that a great variety of causes, mechanical and physiological, sudden 
and gradual, may be blamed for the intracranial disturbance. Let me 
repeat, however, that simply the diminution alone in the intracranial 
quantity of blood is not to be regarded as the whole of the pathology 
of the trouble, or as the sole cause of its symptomatic exhibitions. 

Pathology and Pathogenesis. — Macroscopically the brain looks 
pale and whitish. There is a noticeable deficiency in the number of 
puncta vasculosa in the white substance. The gray matter looks whiter 
than it should and its vascularity seems diminished. The membranes 
are pale and there is an effusion of serum in the pia mater. Both inside 
and outside of the ventricles the cerebrospinal fluid is slightly in- 
creased. Paleness and excessive moisture are the chief gross appear- 
ances. Microscopically the nerve cells are said to be changed, are un- 
duly translucent or granular ; while the vascular walls are somewhat 
degenerated and thickened in some cases. These appearances may be 
general throughout the brain or local, according to the nature of the 
primary cause. 

Symptoms. — These are practically the same for all cases, though 
in detail they will vary widely, according to whether the anaemia is 
general or local, primary or secondary, slight or severe. " A 
simple attack of syncope illustrates well the main features 
of the clinical picture. The patient, suddenly or gradually, 
experiences a sinking sensation, his head gets light, spots 
float before his eyes or his vision gets clouded, he feels dizzy and sud- 
denly weak, his heart seems to flutter, his breathing is somewhat sigh- 
ing and heavy, his ears buzz, he is nauseated and may even vomit. He 
falls or is quickly placed upon a chair or couch. His eyes close and 
his consciousness vanishes. In a few moments he comes to, is dazed 
or slightly delirious, manifests apathy and a desire for sleep. The 
pupils are contracted though later on they may be dilated. In severer 
cases, such as follow sudden loss of blood, the symptoms are more 
swift in onset and more profound. There is a sudden flash of light 
before the eyes, followed by darkness, a quick loss of consciousness, 
vomiting and falling. The pulse is weak and hurried; the respirations 
are labored, shallow and sighing; the skin is moist and cool, and the 
pupils are dilated. The reflexes arc all annulled, the pulse grows 
slower and feebler and in some cases the patient dies in a convulsion. 
In other cases spasms pass over the body and the patient awakens 
momentarily delirious and complaining of severe headache. Some- 
times the consciousness vanishes only when the patient attempts to 
sit up, being present as long as he keeps the recumbent position. \ 
had a case of profound neurasthenic anaemia in a woman who while 
perfectly flat on the back swooned away every few moments. Some 
of the severe hemorrhagic cases may continue from several minutes 
only to an hour. They are dangerously near death and one cannot 
at times foretell the outcome. 

In general chronic anaemia there is a general sluggishness of the 
cerebral processes with a tendency to functional vagaries, paresthesia 
and even hallucinations. Irritable weakness of the nerve elements Is 
the nearest we can come to an explanation of the pathogenetic phe- 



824 THE NON-NEURONIC DISEASES 

nomena. These patients are drowsy, indifferent, lack initiative force 
and staying qualities. Their memories are weak, the volition lacks 
vigor, the imagination and intellect will only work under a vigorous 
spurring. They are prone to sleep and yawn and are regarded as splen- 
did illustrations of laziness. Everything but to sit and read, is an 
effort to them, especially all mental exertion. Sometimes they arouse 
into tremendous irritability and excitement over trivialities and com- 
plain of every noise and unusual ray of light. They are decidedly 
neurasthenic. Heaviness of the head, insomnia at night, occasional 
spells of syncope, mistiness before the eyes and vertigo upon every sud- 
den movement, all relieved by lying down, are the lot of these suffer- 
ers of anaemia from chlorosis, frequent hemorrhages, pernicious 
anaemia and similar causes. 

Marshall Hall has applied the adjective hydrocephaloid or hydroen- 
cephaloid to a type of cerebral anaemia seen in children with 
prolonged diarrhoea. The patient lies in a semicomatose condition with 
eyes partially open, pupils contracted, fontanelle depressed, with 
symptoms later on resembling those of basilar meningitis, such as 
dilatation of the pupils, convulsions, strabismus, retraction of the head 
and death in profound coma. 

Anaemia is probably at the bottom of the cases in which delirium 
is associated with marasmus and extreme inanition. In the cases 
which in the past have been spoken of as oedema of the brain, anaemia 
is in all likelihood the fundamental pathological basis of the symptoms. 

As a part of the anaemic state, malnutrition and intoxication, as 
I have already intimated, may play the chief role. 

Diagnosis. — Is easy when all attendant circumstances are taken 
into account. The immediate cause, the underlying cachexia, the char- 
acter and distribution of the general symptoms in general anaemia, and 
focal symptoms in local anaemia, and the absence of all other signs of 
organic disease of the brain will form the basis of a correct diagnosis. 
Congestion of the brain may in a few instances simulate anaemia, and 
organic disease may have anaemia as a part of its pathological com- 
plexus. These, however, with care are easily differentiated. 

Prognosis. — This is generally favorable in mild cases. Cases 
due to heart lesions, exhaustive hemorrhages and other grave condi- 
tions, with coma, are dangerous and too often fatal. Serious signs 
of trouble are convulsions, pupillary dilatation and light iridoplegia. 
The hydrocephaloid cases of children are usually favorable under 
prompt and proper treatment. Visual disorders sometimes remain 
after severe anaemic spells. 

Treatment. — First and foremost is to force the blood back into 
the brain as quickly and judiciously as possible. In acute cases the 
patient should be placed with the head downwards. In chronic cases, 
I usually always have them occupy a bed with the toot of it slightly 
elevated on bricks. In the acute cases the limbs may be slightly bound 
or an Esmarch bandage may be temporarily applied. Transfusion may 
have to be employed in some cases. The cause of and character of 
the attack must always be taken into account. If the heart has sud- 
denly failed, proper stimulants in the way of alcohol, ammonia salts. 



THE NON-NEURONIC DISEASES 825 

aromatic spirits of ammonia, must be administered. If there is a 
vasomotor spasm, amyl nitrite and nitroglycerin are called for. A 
few drops of the former may be inhaled from a handkerchief, while 
the latter is to be given hypodermically. They should not, of course, 
be given together. 

Cold and heat to the skin, tickling, faradization, sinapisms,- am- 
monia inhalations may do in most cases of simple syncope. 

Artificial respiration may be required in some severe cases. 

The general management of the cases involves the treatment of 
the primary disease and the improvement of the general anaemic con- 
dition. The focal anaemias are referred to under the head of cerebral 
softening or encephalomalacia. 

CEREBRAL HYPEREMIA. 

The statements previously made in regard to the possibility and 
frequency of circulatory disturbances in the brain apply to hyperemia 
as well as to anaemia. In the past too much was assumed and too 
definite a description of the symptomatology of a supposed cerebral 
congestion was promulgated. Actual facts were wanting and theories 
ran riot. On the other hand to-day in some quarters there is too 
strenuous a denial that cerebral congestion ever occurs or presents dis- 
tinctive symptoms. Both logic and data proclaim that the condition 
does sometimes occur and that certain special manifestations are the 
direct outgrowth of the condition. We can therefore reasonably oc- 
cupy a middle ground and wait for further observations to clear up 
many things that are still unaccountable. 

The essential fact in cerebral hyperaemia is, of course, the exces- 
sive amount of blood in the cerebral vessels. This tells, however, only 
a part of the story. Much is still within the dark in regard to the 
mechanism of the production of this congestion and in regard to asso- 
ciated conditions upon which the symptoms may depend for aught we 
know, such as the composition of the blood, the speed of its flow, the 
influence of its altered pressure, etc. Changes of quantity alone are 
gross and unsatisfactory grounds whereon to explain the delicate 
changes of nervous activity. 

It has been declared that there is a permanent form of cerebral 
congestion caused by continuous mental exertion, by certain constitu- 
tional plethora and by some other conditions. This is very question- 
able, however, and even were the possibility and probability of such to 
be granted, it would still be hard to say what in any particular indi- 
vidual should be the normal quantity of the blood in the encephalon and 
at what point it ceases to be normal and becomes a! (normal or true 
hyperaemia. Clinically we are much more concerned about the tem- 
porary or transient cerebral congestions, as they at least exhibit 
lines of demarkation, coarse to be sure at times, whereby we can 
distinguish the normal from the abnormal. 

Temporary hyperaemia of the brain may be active and arterial <t 
passive and venous. The former is often the beginning of an inflam- 
mation ; the latter is frequently recognized as hypostatic congestion. 



826 



THE NON-NEURONIC DISEASES 



Etiology. — The causes of active congestion of the brain are both 
numerous and diverse. Among them we recognize a general plethoric 
condition that is disturbed and sends a flush of blood to the head ; the 
beginning of certain febrile states with its varied agents such as in- 
fection, elevated temperature, nervous irritability ; cardiac over-activity 
from whatever cause, organic or functional ; cold to the skin and a con- 
traction of the peripheral arterioles ; a dilatation of the arterioles of 
the brain by certain drugs such as amyl nitrite, nitroglycerin and alco- 
hol, possibly by mental emotion and other nervous influences, as in 
neurasthenia, hysteria and perhaps in certain vasoneurotic diseases 
like exopththalmic goitre ; suppression of certain customary discharges ; 
strains and violent muscular exertion, etc. Insolation symptoms have 
been attributed to cerebral congestion. 

Any mechanical obstruction to the return flow of blood from the 
head will cause passive cerebral congestion. It is generally therefore 
a chronic condition and is seen sometimes in tumors of the neck, new 
growths in the mediastinum, in pulmonary emphysema and in uncom- 
pensated mitral stenosis. Tight bands about the neck, collars, strain- 
ing,- coughing, sneezing, playing upon wind instruments, and other 
severe muscular effort may cause a temporary congestion or intensify 
one already produced by other factors. In addition to the obstruc- 
tions thus caused in the superior vena cava and veins of the neck, 
the sinuses and veins of the intracranium itself may be blocked by 
thrombosis and other pathological conditions. In certain states of the 
constitution, even the retention of the horizontal attitude may delay 
the return of the blood. 

Pathology and Pathogenesis. — The post-mortem findings in 
cerebral hyperaemia are so indefinite that one can hardly construct a 
pathological picture. The contents of the vessels vary enormously 
and quickly by both ante and post-mortem changes in position and as 
a result of other unknown factors. In suffocation, for example, the 
veins are clearly engorged and yet after death the brain is found to 
be anaemic. Active hyperemia is practically never seen after death 
and so long as it does not run into inflammation, it leaves no signs of 
its former presence. In a few cases the veins of the cortex have been 
distended and the arteries at the base and about the Sylvian fissure 
were full of blood. Mere post-mortem gravitation may have had some- 
thing to do with this ; it is certainly no evidence of what may have 
been the condition during life. In some cases there are bulgings of 
the vessels, blood pigment in the sheaths and minute spots of extrava- 
sation. The value of these as findings is uncertain. In a word then, 
there is no known definite, uniform pathology of cerebral hyperaemia. 

Symptoms. — Leube believes that it is not possible to make a 
diagnosis of pure cerebral congestion, as he contends that the symp- 
toms usually attributed to it are of toxic origin. Osier declares that 
as a separate clinical entity, congestion of the brain rarely comes un- 
der observation. Its symptomatology is certainly very obscure and 
indefinite. Some writers have associated it with throbbing headache, 
delirium, fever, insomnia and convulsions. Mental activity and ex- 
citement, even mania, have been attributed to it. On the other hand 



THE NON-NEURONIC DISEASES 827 

It has been blamed for torpor, dullness of intellect and terminal coma. 
All grades of cases are supposed to exist. In some the face merely 
.flushes up and feels hot, the conjunctivae become red, the temples throb, 
.the eyes flicker, the head aches a little, the mind is dazed and more or 
less nausea and dizziness are present. A full meal, an alcoholic drink 
or a sudden muscular exertion will in neurotic and predisposed plethoric 
people produce such a general exhibition. In severer cases, con- 
sciousness may be profoundly disturbed. Mania and fever are said 
to occur. Meningitis seems to be about to declare itself when after a 
short time all of the symptoms gradually or suddenly subside. Para- 
lytic and apoplectic forms of the trouble have been related. Hemi- 
plegia, aphasia, unilateral convulsions and death have been credited to 
it because, forsooth, no changes of any sort were to be discovered in 
the autopsy. I am inclined to think that some form of virulent intox- 
ication, such as we see in some forms of Landry's paralysis and 
delirium grave, rather than mere congestion is the pathogenetic ele- 
ment in these cases. 

Stupor, insomnia, mental dullness, confusion of mind are among 
the manifestations that have been assigned to passive congestion. 
These are all uncertain, however, and it is to be remembered always 
that the symptoms may belong to the original disease, as, for instance, 
the tumor, the heart disease, upon which the hypostatic congestion in 
part depends. 

Prognosis. — This is favorable so long as the case is one merely 
of congestion. If there is disease of the heart, of the arterial walls, 
hemorrhages, embolus, thrombosis and other complications may arise 
or already be present that will make the outlook in cerebral congestion 
-a matter of some serious moment. Passive congestion takes its prog- 
nosis from the cause upon which it depends. It is bad, of course, in 
tumors, aneurisms and valvular lesions of the heart. 

Treatment. — Prophylaxis is important; stimulants, over-exertion, 
■exposure, mental excitement and dissipation and excesses of all kinds 
must be avoided. The life must be a regular tonic one, including sys- 
tematic exercise, plain, light food, plenty of sleep and fresh air, with 
attention to all the functions of the skin, bowels and kidneys. It must 
he even in all things. Sudden changes are provocative of congestion 
in those who are predisposed. 

In the attack the patient should not lie down. The bowels should 
oe acted upon promptly by an enema, calomel or even croton oil. 
The head should be rendered cool with an ice bag or cold water coil, 
while the feet are placed in hot water alone or with mustard, or wrap- 
ped in hot cloths. Cupping to the sides of the spine, mustard to the 
nape of the neck or leeches to the temples, mastoid bones or back of 
the neck should be though of. Venesection may be advisable, if the 
heart action and general strength do not contraindicate it. Medicines 
are of little avail, though ergot and aconite have been used. 

The other treatment of the trouble, whether active or passive, in- 
cludes symptomatic measures and means to remove the underlying 
cause so far as that is possible. 



828 THE NON-NEURONIC DISEASES 

CEREBRAL HEMORRHAGE. 

An intracranial hemorrhage may occur into the membranes of 
the brain (meningeal hemorrhage) or into the substance of the brain 
(cerebral, medullary, pontile or cerebellar hemorrhage). 

Cerebral hemorrhage is the most frequent and the form that is 
meant when the term hemorrhagic apoplexy is used. The other forms 
of the trouble will be found discussed under appropriate headings else- 
where. 

Etiology. — Disease of the bloodvessels underlies cerebral hemor- 
rhage, hence all factors that tend to the development of such a disease 
and all agents that cause a sudden rupture in the diseased vessel wall 
constitute its chief etiological forces. The former may be referred to 
as the predisposing causes, the latter as the exciting. 
Among the former age, sex, climate, heredity, previous state 
of health and mode of life, exercise a significant influence. 
Hemorrhage may occur at any age but is most frequent at that time of 
life when the bloodvessels are subjected to strains which their debil- 
itated and diseased condition renders them less able to withstand. 
Four-fifths of all the cases therefore occur after forty years of age 
and the liability to it increases with each decade thereafter until about 
the age of eighty when it seems to diminish markedly. Between the 
ages of ten and fifty an apoplectic stroke from hemorrhage is a com- 
parative rarity. The accidents of birth increase slightly the liability- 
of infants. In extreme old age it is not so frequent as is commonly 
supposed, most of the strokes then being due to thrombosis and sec- 
ondary emboli from disease of the vessels. Men, on account of their 
more strenuous lives and greater addiction to alcohol, are somewhat 
more attacked by it than women. The occurrence of more cases in 
the haunts of civilization, among peoples living in the temperate zone, 
in cold weather and at high altitudes is easily accounted for. Strain 
and strenuosity are here more in evidence and all those predisposing 
and exciting influences about to be mentioned. 

It has long been imagined that a tendency to apoplexy ran in cer- 
tain families. There is indeed a slight hereditary influence exerted 
through the vascular system. It is about equal in significance with that 
other time-honored notion that apoplectic individuals possess a partic- 
ular type of constitution, including a short, stocky neck, a florid coun- 
tenance and a stout, plethoric body. As many cases are due to arterio- 
sclerosis, those factors that tend- to the production of this condition are 
important. They include the abuse of alcohol, syphilis, gout, over- 
indulgence in eating with lack of exercise, over-exertion and similar 
agencies. Intoxications and infections predispose to hemorrhage. It 
has followed lead poisoning, rheumatism, the acute infectious fevers. 
Certain conditions of the blood as in purpura, profound and pernicious 
anaemia, leukaemia favor multiple cerebral hemorrhage. Nephritis 
with hypertrophy of the left ventricle of the heart, especially if uncom- 
pensated, must be closely watched as a particularly influential factor. 
Arteritis, atheroma of the arteries, miliary aneurisms, and a fatty con- 
dition of the vessels are all elements in the causation o\ cerebral hem- 



THE N0N-NEUR0NIC DISEASES 829 

orrhage. Numerous are the causes therefore of arterial disease. This 
condition alone, however, probably never provokes a hemorrhage. 
Some sudden strain or other exciting cause must usually operate in 
conjunction with the disease of the arterial system. Among such ex- 
citing causes, numerous as they are, may be mentioned sudden phys- 
ical exertion, like running for a car, climbing a steep hill or riding 
horseback, sudden anger, violent coitus, cold bathing, coughing as in 
pertussis, or the overloading of the stomach with food and drink and 
straining at stool. I have seen it follow a late hearty supper after 
which the patient had retired and gone to sleep. In these cases it may 
be true, as Gowers suggests, that the recumbent posture retards the 
flow of the blood from the brain. Injuries to the head may in excep- 
tional cases provoke a cerebral as well as meningeal hemorrhage. 

To sum up then, the varied etiology of cerebral hemorrhage may 
be classified under the two great sets of causes, the predisposing and 
the exciting. The former include certain familial and temperamental 
traits, certain constitutional cachexias and diseases, and certain definite 
pathological changes in the walls of the arteries ; the latter take cog- 
nizance of a thousand and one physical and mental strains and shocks. 

Pathology and Pathogenesis. — The pathology of cerebral 
hemorrhage resolves itself entirely into the disease of the bloodvessels. 

Atheroma is the most common affection of the cerebral arterial 
system. It affects, however, the larger vessels only and is observed in 
about one-fifth of all the cases. It leads indirectly to the hemorrhage 
by impairing the resiliency of the vascular walls. 

Degenerative arteritis leading to the formation of miliary aneur- 
isms is the immediate cause of the majority of hemorrhages. These 
minute dilatations measure from i-ioo to 1-25 inch (one-fourth to one 
millimetre) in diameter, rarely number more than a hundred, and ap- 
pear most numerous on the arterioles supplying the central ganglia. 
There is some doubt as to the exact nature of their origin. They arc 
certainly not inflammatory. Charcot thought they were associated 
with a periarteritis and were due to changes in the adventitia. Later 
investigators believed that the alterations were in the intima. The 
probability is, from the most recent studies, that the muscular coat is 
the primary seat of the disease process. This atrophies and disinte- 
grates, ultimately causing the entire vessel wall to be degenerated and 
excavated. The periarteritis noted by Charcot is in all likelihood a 
secondary process. These little fusiform and sacculated bodies arc 
not encountered as a rule prior to the fortieth year ; after that they in- 
crease in number with each advancing year, showing that they belong 
exclusively to the degenerative period of life. They must not be con- 
fused with simple excavation of the lymph sheath from an effusion of 
blood. Arteriosclerosis may or may not be associated with them. 
While in the great majority of cases their rupture is the immediate- 
source of the hemorrhage, they are not an absolute requisite for such 
a disaster. 

Fatty degeneration of the walls of the cerebral arterioles occurs 
in marasmus, post-infective states, leucocyt hernia, purpura and similar 
•diseases and is sometimes a cause of hemonhagc. 



83O THE NON-NEURONIC DISEASES 

Small hemorrhages undoubtedly occur sometimes as the result of 
mere diapedesis, the walls of the vessels having been rendered more 
permeable in renal disease, severe anaemia, and various infections and 
intoxications. 

The location of the hemorrhage is a matter of some moment. The 
most common is in and about the basal ganglia. In seventy-five per 
cent, of all cases miliary aneurisms develop most profusely upon the 
Icnticulo-striate and lenticulo-optic arteries. After the middle cere- 
bral arteries, the anterior cerebral and posterior cerebral are most 
affected. 

Twenty per cent, of all the hemorrhages within the cranium occur 
in the vicinity of the corpus striatum. The favorite locations in order 
after this are the meninges and cortex, optic thalamus, internal and 
external capsules, centrum ovale. The size and arrangement of the 
arteries in these respective areas have much to do in determining their 
relative importance. The cortical arteries, for instance, are abund- 
ant and richly terminated in a network, whereas the central arteries 
are pure terminal arteries of large calibre and spring from their parent 
stem at right angles. This makes a difference in the pressure to which 
they are relatively exposed. 

The hemorrhage may be small and limited to the striate body or 
internal capsule ; more generally it extends, if large, somewhat into 
the centrum ovale, the lateral ventricle or the insula. It is rare for a 
hemorrhage to be confined to the centrum, or to originate in the ven- 
tricle. The blood in ventricular hemorrhage may flow into all of the 
ventricles and form a perfect mould of them This is the apoplcxic 
fondroyante of the French authors. 

In ordinary cerebral hemorrhage the clot varies greatly in size 
and shape. In insular hemorrhage it may attain the size of a man's 
fist and be irregularly round in shape ; in cortical hemorrhage it may 
be flat and diffuse though it is more often small and multiple. In the 
various diatheses and post-infectious states it is apt to be small and 
multiple. In a few days the clot begins to soften, changes begin to 
take place in and about it, inflammation occurs around the apoplectic 
area and a wall is created inclosing it in a cyst along about the twen- 
tieth or thirtieth day. The contents of the cyst undergo further de- 
generative changes, a transparent fluid fills it and perhaps fibrous tra- 
becular run across it. The age of the lesion can be fairly well deter- 
mined by the decoloration of the exudate, the swelling, the atrophy of 
the red corpuscles and the nature of the pigment. On the third day 
appear only cells with blood-corpuscles. Free pigment is seen about 
the eighteenth day and after the sixtieth. It takes about four weeks 
for the cyst to form, and ten days more for it to begin to contract. 
Complete cicatrization is rare. Either a small cyst remains with semi- 
fluid contents or in the event of no cyst having formed the connective 
tissue proliferates and a small pigmented sear is left. 

Secondary degenerations begin about the tenth or fourteenth day 
and vary, according to the location of the hemorrhage and the particu- 
lar cells and their axones that have been damaged. In old hemiph 
cases thev have been seen to extend nearly all the way down the cord. 



THE NON-NEURONIC DISEASES 83 I 

Symptoms. — There may be slight premonitions of cerebral hem- 
orrhage, though as a rule prodromata are more common in embolism 
and thrombosis. The patient may experience a little dizziness, full 
feeling in the head, headache with episfaxis and disturbed heart action, 
and bad dreams at night. A little numbness of the hand and foot of one 
side may be complained of. All this is rare, however, in hemorrhage. 
As a rule the patient is stricken suddenly while he is at his usual avoca- 
tions or after some unwonted mental or physical strain. The stroke 
having occurred, its symptomatology may be conveniently studied 
under two groups of phenomena — namely, those of the actual apoplectic 
insult and those of the resulting paralysis. Usually suddenly, some- 
times gradually, the patient is rendered unconscious. He falls or is 
caught in time to be assisted to a couch. The coma is in a few minutes 
profound and the patient resembles an individual in the deepest slum- 
ber. He cannot be aroused. His breathing is heavy and slow. The 
cheeks puff in and out with the respirations. The latter are noisy and 
stertorous and may even assume the Cheyne-Stokes character. The 
chest movements are restricted, especially on the side that is paralyzed. 
The face appears flushed, sometimes cyanotic. The pupils are dilated 
and unequal and in the coma irresponsive to light. The limbs are limp 
and dead. If they are slightly raised and then released, it will be 
noticed that they fall heavily on the paralyzed side, but somewhat more 
slowly on the opposite side. The paralysis is positively flaccid and the 
deep reflexes are absent, as well as the cutaneous peripheral reflexes. 
In most cases, especially the foudoyant apoplexies, the coma pre- 
cedes the paralysis. In other cases the gradual approach of the paraly- 
sis is accompanied a little later by unconsciousness. In rare instances 
there may be little or no unconsciousness or the patient may awake 
from a nap to find himself hemiplegic. Swallowing is not performed 
in the comatose stage and is extremely difficult even after the return of 
consciousness. Involuntary micturition and evacuation of the bowels 
sometimes occur in the coma. The pulse is generally tense, full and 
slow. The temperature is normal or subnormal. The head and eyes 
are strongly turned toward the side of the lesion. In some cases gen- 
eralized convulsive movements occur. Gradually in the course of a few 
hours, or even sooner, the coma wears away, the patient opens his 
eyes, tries to speak, and exhibits emotion upon the realization that he 
is paralyzed. Such in brief is the clinical picture of the average stroke 
of apoplexy. Some of its details are deserving of further discussion. 

As I have already intimated, the sudden unconsciousness is the 
most striking feature. Its association with the paralysis makes it 
pathognomonic of cerebral hemorrhage. It varies in depth and dura- 
tion and bears no proportional relationship to the paralysis. It may be 
very slight, while the latter is severe. Its onset is often immediately 
preceded by intense vertigo, headache, fullness of the head and blurring 
of the vision. Things swim before the eyes and the world seems to l> 
going topsy-turvy. It usually lasts from a few minutes to a few hours. 
The restoration to consciousness is more or less rapid and complete, 
though a state of somnolence may follow for some time. The coma 
is believed to be due to the sudden disturbance of the circulation, 



832 THE NON-NEURONIC DISEASES 

(anaemia) and to the molecular concussion throughout the entire brain, 
provoked by the abrupt outpouring of the blood. 

The paralysis, like the coma, varies in different patients according 
to the extent, location and rapidity of the hemorrhage. It is always 
of the hemiplegic or facio-brachio-crural type and is on the opposite 
side of the body from that of the hemorrhage. It involves most the 
finer complicated movements, hence the hand and arm are more affected 
than the foot and leg, and both extremities more than the face. Mus- 
cles that have a bilateral representation in the brain and work on both 
sides of the body in unison are but little affected ; hence the respiratory 
muscles, those of the abdomen and of the eyes soon recover from the 
first shock. Dysarthria may occur from the implication of the finer 
movements of the muscles of articulation. This must be carefully dis- 
tinguished from the aphasia that occurs in right-sided hemiplegia. 
The lower part of the face is always more involved than the upper, a 
differential indication of facial palsy of central origin. The face is 
asymmetrical, the corner of the mouth droops, the naso-labial crease is 
obliterated and the saliva oozes out on the paralyzed side. Deglutition 
is difficult. The laryngeal muscles are not particularly involved. 

With the onset of the coma the temperature usually falls one or 
two degrees. In a few hours it rises to normal or even passes the nor- 
mal point. On the paralyzed side the temperature is usually higher 
than on the other side. If the temperature remains subnormal, or, on 
the other hand, if it takes a rapid rise to 102 degrees or 103 degrees F., 
the coma continuing, death is near at hand. Just before the fatal issue 
the temperature may sink again. 

Vomiting occurs in cerebellar hemorrhage, but very rarely in 
cerebral hemorrhage. 

The conjugate deviation of the head and eyes in the majority of 
cases is toward the side of the hemorrhage. In other words, the patient 
seems to stare in the direction of the lesion. In exceptional cases, es- 
pecially when there are unilateral convulsions or spasms, or when early 
rigidity occurs, the conjugate deviation of the head and eyes may be 
away from the lesion and toward the paralyzed side, or more accurate- 
ly, convulsed side. As a rule this symptom disappears with the wear- 
ing away of the coma. 

For the first day or so the amount of urine passed may be larger 
than normal and it may contain albumin and sugar. 

The sequence of events in and immediately after the stage of seiz- 
ure varies considerably in different individuals and depends upon the 
extent and severity of the hemorrhage. In a few rapidly fatal cases, 
especially when the blood has broken into the ventricles, the patient 
fails to emerge from the coma, the respiration assumes the Cheyne- 
Stokes character, the temperature ascends to 103 degrees F. or higher. 
the pulse beats violently and the patient dies in a day or two with 
hypostatic pneumonia. In another class of cases, fatal but more tardily 
so, consciousness returns partially, mild delirium occurs, with head- 
ache, restlessness and anxiety. With the reaction period setting in in 
about forty-eight hours and continuing for a week or more, the tem- 
perature, after remaining normal for a time, rises, and pneumonia 



THE NON-NEURONIC DISEASES 833 

develops and kills the patient in a state of unconsciousness. These 
cases may last even as long as two months. Early rigidity develops in 
their paralyzed limbs, serious trophic changes occur, such as sloughing 
and vesicular formations, and perhaps the congestion at the bases of 
the lungs. In the favorable cases, which happily constitute the larger 
number, the initial coma disappears in a few hours, leaving the mind 
entirely unaffected, or at the worst only weak and confused. The 
deviation of the eyes and the temporary ptosis pass away with the 
coma, the sound side of the body resumes its proper activity, the 
paralyzed side shows a slight tendency toward rigidity with return or 
even slight increase of the deep reflexes, the temperature, the pupils and 
respirations return to their normal condition. A slight febrile reaction 
with some temporary constitutional disturbance accompanying the in- 
flammatory changes in the apoplectic area, and the absorption of the 
blood may occur in a week or so and then pass away, leaving as the 
prominent and almost sole constituent of the clinical picture the hemi- 
plegia with aphasia when it is on the right side in right-handed individ- 
uals, or without aphasia when it is on the left side. 

Complete hemiplegia is of the facio-brachio-crural type and in- 
volves the arm more than the leg, and the leg more than the face. In 
partial hemiplegia any one of these members may be the seat of the 
paralysis. So dominant and all-engrossing is this one symptom of this 
so-called chronic stage of the disease, that the patient is in common 
parlance referred to as a "hemiplegic." He enters upon this role 
usually about a month after the stroke and when all of the other symp- 
toms have vanished or diminished to such a degree as to be quite un- 
noticeable. 

It is usually stated that the ends of the extremities are more dis- 
tinctly affected with paralysis* than are the segments nearer the trunk. 
The difference is only apparent, however, because in this as in all 
cerebral palsies the more the movements are complicated and the more 
they are related to the higher intelligence normally, the more they are 
affected when paralyzed. The loss of power moreover involves seg- 
ments of the body rather than individual muscles ; movements rather 
than special anatomical structures merely. 

Movements that normally depend upon muscles that act bilaterally, 
such as those of respiration, phonation and facial expression, are but 
slightly, if at all, affected. Each side here is probably better repre- 
sented bilaterally in the brain than are the movements of the arms 
and legs. That there is some bilateral representation of the latter in 
the cortex is shown by their tendency to act together in untrained nor- 
mal individuals, and by the fact that even in true hemiplegia some 
weakness is observed on the sound side. The movements of the lower 
part of the face, as in all central facial palsies, are more involved than 
those of the upper part. The frontal muscles and the orbiculares palpe- 
brarum continue to act, while the cheek, the side of the nose and the 
corner of the mouth are almost or quite immovable. The tongue is pro- 
truded towards the paralyzed side because the involvement of the mus- 
cle on that side of it leaves the muscle of the other side without its nor- 



834 THE NON-NEURON IC DISEASES 

mal opposition. The soft palate may be slightly pendant, but the mus- 
cles of deglutition are not seriously involved. 

On account of the paralysis of the tongue, lips, cheek, etc., there 
is a true paralytic dysarthria, which must not be confused with the 
disturbance of speech known as aphasia. I have seen such an error 
made. In aphasia wrong words or no words at all are uttered ; the 
few that may be employed are not affected in any way by articulation ; 
the trouble is one of psychic origin rather than of mere muscular in- 
efficiency. On the other hand, in paralytic dysarthria there is no lack 
of words and speech, no utterance of wrong words, but rather a bad 
and inefficient articulation of them. The trapezius is liable to be 
included in the paralysis. Certain automatic movements, like crying 
and laughing, are usually performed when the face cannot be moved 
voluntarily. 

The paralysis in the limbs may be partial or complete. In the for- 
mer condition a slight degree of activity in certain directions is re- 
tained. The fingers in a few days or weeks can be slowly and partially 
flexed ; the arm can be slightly bent at the elbow ; and the whole 
extremity can be drawn over towards the body. The movements are 
all feeble and sluggish, however, and performed clearly with a heroic 
effort. The flexors, as a rule, show more of a tendency to recover than 
do the extensors. A great number of variations obtain in regard to the 
distribution of the paralysis. As a rule the leg recovers much more 
than the arm and nearly always so much that walking after a fashion 
is possible. In many cases only the face and arm remain paralyzed. 
In others the face recovers and the arm remains paralyzed more than 
the leg. It is very rare for the face and arm to escape or recover 
while the leg alone remains involved. In mild cases many kinds of 
coarse work can be done with the hemiplegic hand and arm ; usually 
the finer kinds of work requiring nice adjustment and coordination, 
such as writing, playing upon musical instruments, etc., are impossible 
or extremely difficult. It is rare for these finer movements ever to 
become possible again unless the case has been unusually mild and a 
complete recovery obtained. The inability to write must be carefully 
examined in some cases so as not to be confused with agraphia. The 
distinction is usually easily made and demands only a little ingenuity in 
applying the proper tests. 

The gait of the hemiplegic is characteristic and is to be carefully 
differentiated from that of the ataxic and spastic paralytic. It depends 
upon the motor paralysis, the slight rigidity or contracture and the 
slight weakness and wasting of the muscles. In severe cases it is 
typical. The support of the body is placed well upon the sound limb; 
the paralyzed member, slightly rigid and even contractured in old cases, 
is dragged forward in a sort of a half-circle around the sound member 
as an axis, the pelvis drawn up a trifle on the affected side and the foot 
planted forward upon the entire sole without the toes having once been 
clearly lifted from off the floor. The simple manoeuvre of stepping" 
sidewise will usually discover the hemiplegic side in those very slight 
cases, as in some instances of senile hemiplegia, in which the gait is not 
very obviously altered. 



THE NON-NEUKONIC DISEASES 835 

After the first few weeks the paralysis assumes the spastic type. 
In rare and unaccountable cases it may remain flaccid throughout. 
From being absent during the comatose stage., the reflexes become 
normal and ultimately exaggerated. Even ankle-clonus may be present. 
Sometimes the exaggeration of the reflexes is bilateial, though it is 
always more exaggerated on the paralyzed than on the well side. The 
superficial reflexes usually recover in part, though they are always 
more or less diminished. The electrical reactions are normal ; and 
there is no true muscular atrophy, only a slight wasting from non-use. 
An early rigidity appears in the muscles during the reaction period. A 
late rigidity with contracture and deformity appears as the accom- 
paniment of the secondary degenerative sclerosis in the pyramidal 
tracts. These late contractures affect the hand and arm more than the 
leg, are somewhat painful and remain permanently. As a result the 
elbow is partially flexed and the fingers bent. I have seen during the 
development of this late rigidity violent muscular spasm or cramp 
with most excruciating pains. In a few instances there has been no 
rigidity or contracture, but tremor, post-paralytic chorea, athetosis, 
arthropathy and even muscular atrophy have been observed on the 
hemiplegic side. 

The sensory phenomena of cerebral hemorrhage and hemiplegia 
are not in any way pathognomonic. Hemianesthesia may occur with 
the paralysis if the posterior part of the internal capsule is injured. 
This, however, is rarely total. Usually it passes off quickly and leaves 
only a partial anaesthesia or rather hypsesthesia in various parts of the 
affected side. Much more common are the various paresthesias, show- 
ing irritation of the sensory tracts or cortex. Pain is often com- 
plained of, especially of a burning character, about the articulations. 
Xumbness is the more common form of paresthesia spoken of. The 
special senses as a rule escape all involvement. Occasionally, how- 
ever, hemiopia on the side of the lesion has been noted and the taste, 
smell and hearing -have been blunted. According to Gowers, hom- 
onymous hemianopsia of the half-fields opposite the lesion is more 
frequent than reports would seem to indicate. If the examiner sud- 
denly brings the finger before the eye in the early stage of the trouble, 
first from one side and then from the other, it will be noticed that the 
eyelids blink when the finger comes from the unparalyzed side, but 
not when it approaches from the other side. 

Trophic manifestations often show themselves early, within the- 
first five or six weeks, in severe cases. The joints become inflamed 
and acute decubitus develops on the paralyzed side of the gluteal re- 
gion. Sloughing in the lower part of the back, which may come on 
as early as forty-eight hours after the stroke, is a very unfortunate 
event. It usually means death. A flushing occurs first, according to 
Charcot, then a violet discoloration, vesicles, ulceration and finally an 
eschar. The hypostatic pneumonia which sometimes occurs is be- 
lieved by some to be a trophic phenomenon. The same may be said 
of the gastric hemorrhages. Hyperidrosis, cutaneous eruptions and 
increased growth of hair have been observed in rare instances. I 



836 THE NON-NEURONIC DISEASES 

have often noted the glossy appearance and cool character of the skin 
in the paralyzed limbs. 

Rare but interesting are the ataxic hemiplegias. Here the hem- 
orrhage has confined itself to the area of the sensory tract and the 
ataxia results from the complete hemianesthesia. The hemiplegia in 
such instances may be absent entirely or only transient. Hemiataxia, 
of course, is the true character of the trouble and its one-sidedness 
readily distinguishes it from all other forms of ataxia. 

It would be extraordinary if so profound a shock as cerebral hem- 
orrhage induces did not affect the mind somewhat. The aphasia, early 
stupor, delirium and somnolence are all partly in the psychic sphere. 
Irritability, emotionalism, failure of memory are some of the more 
specific mental disturbances that occur in the older victims of the dis- 
ease. Marked mental deterioration, irritative epilepsv and terminal 
insanity have been known to follow cerebral hemorrhage, especially one 
of large degree. It is to be remembered that mentalization is sub- 
served by language and that when aphasia is of long duration the want 
of speech may well react upon the mental faculties and cause them to 
deteriorate. The mere realization of the fact that the paralysis is per- 
manent and that the apoplectic danger, as shown by the present attack, 
hangs like the sword of Damocles constantly over the patient's head, 
has its influence in depressing the mental forces. 

The discussion of the symptomatology of other than cerebral 
forms of intracranial hemorrhage will be taken up when the diseases 
of the meninges, pons, medulla, etc., are considered. A word should 
be spoken here, however, in regard to ventricular licmorrhage. As a 
primary condition it is exceedingly rare. Usually the blood enters 
the ventricles by extravasation from neighboring parts of the brain or 
bursts into them suddenly in the course of an ordinary apoplexy. The 
symptoms are always under such circumstances serious and profound. 
The coma deepens, or if it had begun to clear up, it abruptly returns 
and is more profound than it was before. Convulsions sweep over 
all four extremities, followed by complete paralysis. The muscles are 
rigid on the hemiplegic side, or in all four members. The pulse is- 
retarded, respiration is extremely embarrassed, the temperature is de- 
creased and just before death, which usually takes place inside of 
twenty-four hours, the eyes become fixed and staring, the pupils dilated 
and the general appearance of cyanosis and asphyxia occurs. 

Diagnosis. — The physician is rarely confronted with a more im- 
portant problem and one that makes larger demands upon his knowl- 
edge and judgment, than when he is called upon to make a diagnosis 
in an apoplectic stroke. The proper management of the case depends 
at first almost entirely upon whether the stroke is due to hemorrhage, 
embolism or thrombotic obstruction. Moreover, the coma and other 
symptoms of the first stage are simulated by a number of other dis- 
eases that are not apoplectic. And finally there are different degrees 
among the cerebral hemorrhages themselves that must be differen- 
tiated if possible in order to form some opinion in regard to the prob- 
able ultimate outcome. 

While all these questions and distinctions are at times hard to 



THE NON-NEURONIC DISEASES 837 

settle, owing to the multiplicity, variety and great differences in the 
individual symptoms of cerebral hemorrhage, there is a uniformity and 
consistency generally about the clinical picture that, when studied in 
toto, help very materially towards the 'establishment of the diagnosis. 
Coma and paralysis are the two guiding posts that always point unerr- 
ingly to a serious intracranial lesion. The approach of, the character 
of and the associated manifestations surrounding the coma and the 
paralysis are the chief means by which we must determine the nature 
of the lesion producing them. In hemorrhage the onset is sudden 
or with very slight prodromes, and the maximum is attained almost 
immediately. The coma is usually deep and precedes the paralysis. 
The latter at first seems to involve all the limbs, but soon recedes from 
one side. The face, arm and leg of the hemiplegic side are implicated. 
The paralysis is flaccid and complete from the start and is only rarely 
preceded by convulsive movements. The pupils, contracted at first, 
soon become dilated, unequal and irresponsive to light. The flushed 
countenance, puffing cheek, labored stertorous breathing, rapid pulse, 
early subnormal temperature and occasional involuntary micturition- 
and evacuation of the bowels are contributing signs to the completing 
of the clinical picture of cerebral hemorrhage. 

The cases of cerebral hemorrhage that develop slowly, taking a day 
or two for the attainment of their maximum degree of coma and 
paralysis, may be mistaken for thrombosis, especially in the aged with 
atheromatous arteries. So common is this error in diagnosis that I 
am confident the relative proportion of cases of hemorrhage has been 
greatly exaggerated in the reports. A large number of them have been 
cases of thrombosis. Admitting the occasional difficulty encountered 
in making the differentiation, a closer attention to the course of the 
disease and the changes exhibited by the individual symptoms will 
render such errors less frequent. 

There is a group of cases, usually seen for the first time when 
they are comatose, in which the coma comes on rapidly rather than 
abruptly and the paralysis is not as profound as in many other cases. 
( )r the loss of power develops in the course of a few hours and is 
followed by a gradual loss of consciousness. These so-called ingraves- 
cent cases cannot be distinguished usually from cases of embolism or 
thrombosis unless there are some very suggestive circumstances in 
connection with the age of the patient, his constitutional diseases and 
the immediate cause of the stroke. Even then the diagnosis falls short 
of being positive. 

The tvpical cases of cerebral hemorrhage that come on abruptly 
and are in a state of profound coma and paralysis must be differentiat- 
ed from the coma of uraemia, alcoholism, opium poisoning, diabetes and 
syncope. Epilepsy and hysteria must be excluded also. 

In urccmic coma there is no hemiplegia and the pupils are net 
unequal. The coma comes on gradually or less suddenly than it does 
in hemorrhage and is usually preceded by blindness, convulsions and 
vomiting. The temperature is below normal always. A chemical and 
microscopic examination of the urine and the existence of albuminuric 
retinitis, with the peculiar physiognomy that accompanies nephritis, 



838 THE NON-NEURONIC DISEASES 

would, of course, determine the diagnosis. In diabetic coma the breath 
may exhale the odor of acetone. Urinalysis here will also establish the 
nature of the disease. 

Severe alcoholism is not infrequently confounded with hem- 
orrhagic apoplexy, as the records of some of the police stations will 
amply prove. The odor of the breath cannot be taken as a criterion, 
for the patient may have felt the apoplexy coming on and taken the 
stimulant to ward off the sudden weakness or vertigo. In alcoholism 
the coma is incomplete, the pupils are equal, the limbs show no ten- 
dency to a hemiplegic condition, the temperature is not lowered and 
there are some manifestations of delirium. The examination of the 
contents of the stomach, as the patient usually vomits, will strongly 
suggest the length of time the alcohol has been ingested. 

In opium poisoning the pupils are equal and strongly contracted, 
the respirations are slow and there is no true paralysis. 

Epileptic attacks are preceded by a cry. The pupils are equal 
and dilated, the tongue is serrated, the teeth are clenched, and instead 
of paralysis the muscles are in a state of convulsion. Consciousness 
returns rapidly, to be followed by headache and drowsiness. 

Hysteria is so purely psychic that one wonders how the mistake 
can ever be made between it and the coma of cerebral hemorrhage. 
The stigmata of hysteria, such as the anaesthesias, will always be dis- 
covered if sought for in cases of hysterical hemiplegia. 

Syncope is not characterized by complete coma. It depends upon 
an impaired heart action and therefore leads one to examine care- 
fully the pulse, the general hue of the patient and the heart. Moreover, 
syncope is of short duration and is not accompanied by any paralytic 
symptoms. 

In general paresis apoplectiform seizures are not uncommon. The 
history of preceding mental symptoms, headache, elevation of tem- 
perature and preservation of the reflexes are usually enough to indicate 
the presence of encephalitis. 

Perhaps the greatest difficulty in the differential diagnosis of 
cerebral hemorrhage is when an attempt is made to distinguish it 
from an embolic or thrombotic apoplexy. In some cases the differen- 
tiation is absolutely impossible. The history of the case, its mode of 
onset and its associated conditions are most important. 

Cerebral embolism occurs earlier in life than hemorrhage. The 
age of forty is approximately the period before and after which occur 
respectively embolism and hem&rrhage. Embolism is usually asso- 
ciated with heart disease, rheumatism, syphilis or the puerperium. 
Prodromes sometimes, but rarely, precede the apoplectic stroke. The 
coma comes on gradually, is less deep than it is in hemorrhage and as 
a rule follows the appearance of the hemiplegia. The pulse and heart 
action in embolism are weak, in hemorrhage they are strong and vio- 
lent. The face is not flushed, the temperature is not disturbed, nor is 
the coma so prolonged as in hemorrhage. The paralysis comes on more 
gradually, is less complete, is associated with convulsive movements, 
and is more rigid and less widely distributed in embolic obstruction 



THE NON-NEURON1C DISEASES 839 

than in hemorrhagic apoplexy. Infarcts in remote organs and repeti- 
tions of the stroke indicate embolus. 

It is much more difficult to differentiate hemorrhage from throm- 
bosis, particularly as both occur in old age and are dependent upon 
similar diseased states of the blood vessels. Prodromata, often for 
days and weeks, precede the coma, which is apt to be slight in degree 
and short of duration. The succession of slight spells of semi-con- 
sciousness, the irritability, the paraesthesise, the general asthenia, the 
muscular twitchings of thrombosis I have seen diagnosed and treated 
as hysterical. In thrombosis there is psychic weakness, hardness of 
the arteries, evidences of a fatty heart, and absence of stertorous 
breathings, flushed face, temperature phenomena and convulsive move- 
ments of large amplitude. 

Prognosis. — The prognosis of cerebral hemorrhage should al- 
ways be guarded, especially in the comatose stage and until after the 
period of febrile reaction. The size of the hemorrhage, its location and 
the duration of the coma all determine the future outlook. If the coma 
is profound and prolonged three or four days, if it is initiated with a 
subnormal temperature or accompanied by an excessive rise of tem- 
perature, if decubitus or pneumonia appears, or if delirium develops 
and continues, the outlook is bad. 

Ingravescent apoplexy with its progressive somnolence passing 
into deep coma is usually fatal. 

Signs of nephritis, Cheyne-Stokes breathing and symptoms of 
rupture into the ventricles are all bad indications. A history of alcohol- 
ism adds to the gravity of the prognosis. Death under these circum- 
stances may occur anywhere from a few hours to a few days after the 
stroke. 

The larger number of cases of cerebral hemorrhage usually re- 
cover, in part at least, from their first attack. In a few years, three 
to five, they have another attack, from which they die or recover with 
difficulty and more serious residua. Rarely do they have a third or 
fourth stroke. 

A favorable prognosis may be held out if the coma clears up early 
and at the end of the first week there has been no fever or only a slight 
rise of temperature and none of the ill omens referred to above. 

Complete recovery is rare, though improvement may continue for 
two years. 

A hemiplegia that remains the same for one month can hardly 
le expected to improve very much. After a year no further change 
can be hoped for in the great majority of cases. If a return of move- 
ment shows itself within a few days after the stroke, and continues, 
the outlook for recovery from the paralysis is particularly bright. 

Hemiplcgic aphasia dependent upon hemorrhage usually disap- 
pears sooner or later. Partial aphasia, however, may remain perma- 
nently. Initial hemianopsia as a rule disappears after a few days, [f it 
does not it may be looked upon as permanent. 

The power of walking is acquired at various periods in different 
cases. In some cases only a few weeks or even days intervene between 
the stroke and the time when the patient begins moving about. In the 



84O THE NON-NEURONIC DISEASES 

majority of cases, however, walking is not commenced for three or four 
months after the stroke. The gait at the end of a year is apt to be the 
permanent one thereafter. 

Treatment. — As the management of apoplexy, and especially of 
the hemiplegia that follows it, is in the main the same for all forms, 
I will treat of it here in detail and merely refer to the differences in 
the treatment of embolic and thrombotic apoplexy in the next section 
headed cerebral softening. 

The dissimilar modes of first handling the patient demanded in 
cerebral hemorrhage and embolic obstruction enhance a hundred-fold 
the need of care in diagnosing the nature of the lesion. A misjudg- 
ment in the arrangement of the position of the patient may mean death 
instead of life. The administration of a heart stimulant in place of a 
sedative may bring the case promptly to a fatal issue. An unwise 
attempt to evacuate a full stomach may provoke a renewal of the 
hemorrhage. A simple venesection may hasten or retard the end. 
All these points must be quickly and seriously considered, usually in 
the presence of the patient, who will be found surrounded by terrified 
and clamorous friends. 

In considering the general treatment of apoplexy most authors 
begin by dividing the subject into the prophylactic treatment and the 
management of the attack and its sequelae. It had been better, it seems 
to me, if the emphasis had been laid more upon the treatment of the 
respective conditions of hemorrhage and embolism. In the main 
the prophylaxis is about the same for both. 

A quiet life, both physically and mentally, is a desideratum. The 
digestive and nutritive organs should be relieved of strain and encour- 
aged to functionate normally. The emunctories should all be kept 
active to rid the system of deleterious substances. Sleep should be se- 
cured. Mental and physical activity should be evenly balanced. In a 
word, the threatened victim should be induced to lead a life of mild 
and even tenor, devoid of anxiety and brightened by as much happi- 
ness as possible. Beyond this little can be offered in the way of advice 
against an attack of hemorrhage or embolism. 

It is quite otherwise in regard to the attack itself. Xow the advice 
becomes of definite and distinct importance. The differential diagnosis 
must be made as sharply as possible. The suggestions to the nurse 
and attendants must be precise and not open to the least misconstruc- 
tion. The patient when first seen will be almost invariably found lying 
tiat on his back. Position is an important factor, and it behooves one 
to decide quickly how to place the patient to the best advantage. 
Gravity plays a role, though a slight one, in the force of the circula- 
tion ; hence it must be remembered in connection with the nature of 
the lesion. If the case is one of hemorrhage, a half-reclining position 
on one or the other side of the body is the best. Heidenhain recom- 
mends that the patient be put in a sitting-erect position and maintained 
in such an attitude as long as possible. I have seen amelioration of 
the symptoms by this simple manoeuvre. Often the friends standing 
about will strenuously object, but a compromise may be made by prop- 
ping the patient against the overturned back of a chair in a half- 



THE XOX-XEUROXIC DISEASES 84I 

reclining position. While he is in this attitude cold in the form of 
cracked ice should be applied to the head to cause as far as possible 
contraction of the cerebral vessels, and heat to the lower extremities 
to dilate the blood vessels there and so lessen the blood-pressure in the 
brain. The latter may be further accomplished by the cautious ad- 
ministration of a cardiac sedative, such as tincture of aconite or vera- 
trum. 

If the case is one of embolic obstruction the reverse of all this 
should be done. Now we desire to increase the intracranial blood- 
pressure ; for the embolism being already there and beyond the hope 
of immediate removal, it is our object to check its progress and fur- 
ther development by suddenly making it stationary. To do this the 
patient's head should be placed as low as possible. The cold and heat 
may be applied as before, but instead of a cardiac sedative a stimulant 
now acts more favorably, such as alcohol, ammonia, or even small 
doses of digitalis and ether. 

The importance of attending at once to the decubitus of the pa- 
tient is brought out by the fact that undoubtedly some fatalities occur 
from suffocation. Kind friends, not knowing what to do, put the 
patient on his back, with head low, and administer brandy, milk or 
whisky. Very often the tongue is partially paralyzed, as well as the 
pharynx, while the sensitiveness of the buccal mucous membrane is 
lost. Saliva and fluids collect, obstruct and even enter the air-passages, 
setting up inhalation-pneumonia. The obvious thing to do is of course 
to raise the head, place the patient on the side, carefully pull forward 
the tongue, and swab out the mouth with a dry rag or bit of linen 
moistened with some aromatic, antiseptic mouth-wash. 

As the respiratory power is usually diminished, it is important that 
the patient should have all the fresh air possible. Crowding about his 
bed should be forbidden, and the windows even in cold weather should 
be more or less open. Tt may even be necessary to perform artificial 
respiration, this being done with as little disturbance of the patient as 
possible, and only until the respiratory centers have sufficiently recov- 
ered from their shock to resume their normal functions. All con- 
striction about the neck by tight clothing must be removed, so that the 
return of circulation may not be obstructed. To increase the blood- 
pressure within the cranium in embolism, it may be well at times to 
apply the Esmarch elastic bandage to the lower extremities. It would 
be unwise to do this as a routine measure, but its worth in some cases 
cannot be doubted. 

To determine the blood away from the head we have two rapii 
and powerful methods — namely, bleeding and hydragogue purgatior. 
The old-time practice of placing two or three drops of croton oil on the 
back of the patient's tongue is a good one. A brisk enema may be 
employed in some cases, but usually it is too slow in action. The same 
may be said of elaterium. Cerebral congestion is certainly modified 
by quick action upon the circulatory and glandular apparatus of the 
bowel, as can be clearly demonstrated; hence it is a rational con- 
clusion to hold that the same means will be effective in lessening the 
intracranial blood-pressure in hemorrhage. 



842 THE NON-NEURONIC DISEASES 

In regard to venesection, or the abstraction of ten or a dozen 
ounces of blood, there is a wide divergence of opinion. At one time it 
was a routine practice and consequently abused. On the other hand, 
there are those who boast that they never bleed a patient. Of the 
two extremes the latter is the preferable one. The abstraction of a 
few ounces of blood is almost immediately followed by a partial return 
to consciousness, and hence the one-time popularity of the treatment. 
It should be remembered, however, that the heart action in apoplexy 
is usually weakened. Therefore, to still more weaken it by depriving it 
of its natural stimulus, the blood, is hardly a commendable procedure. 
Only in sthenic cases with flushed countenance, full pulsating vessels, 
and a vigorous general physique is venesection to be thought of. The 
thinning of the blood diminishes its tendency to coagulation at the seat 
of hemorrhage and lessens its stimulating power upon the medullary 
cardiac center and heart muscle. In jnost cases these disadvantages 
would so far outweigh the possible little benefit due to the mechanical 
diminution of the intracranial blood-pressure that I am generally op- 
posed to the operation. In the few cases in which I have abstracted 
blood, it seemed to me that the slight benefit and partial restoration to 
consciousness were so temporary as to be without any special value. 
In one case I fear it hastened the end, though both the attendant and 
myself anticipated the best of results. 

All such slow means of withdrawing blood from the head as 
leeches to the temples, mustard to the nape of the neck, blisters, etc., 
may be tried in some cases, perhaps most cases ; for, fortunately, even 
if they are slow, they are not open to such objections as is venesection. 
If they irritate the patient they had better be desisted from, for the 
patient's distress will tend to a return or extension of the hemorrhage. 

Diuretics are judicious, and in this connection it is well to mention 
that catheterization will sooner or later be required in almost every 
case. The bladder is usually paralyzed to a certain extent and fails 
to void its contents. Unless the catheter is promptly and systematically 
used the patient will experience distress, if he does not acquire a 
cystitis. 

The skin should be attended to, and a gentle rubbing of the surface 
of the body with alcohol and tepid water cannot fail to be of some 
benefit. The enormous capillary circulation in the deeper layers of the 
skin may be made to retain a large amount of blood by the application 
of warmth to the body surface. Moreover, the cleansing of the skin 
with warm water awakens the activity of the glandular apparatus, and 
this will aid in determining the flow of blood away from the head. 

It will thus be seen that very active treatment immediately after 
an apoplectic shock is uncalled for. Beyond careful nursing, quietude, 
arranging of the patient's position, attending to the respiration, nutri- 
tion and excretions, the physician can give but little advice. If the 
shock is so severe that death is inevitable, little that art or science can 
do will be of any value one way or the other. The end will come in a 
few days or hours, and though the occasional twitching of the muscles 
of the extremities as a result of the local irritation of the clot may 
awaken false hopes of a return to consciousness, the physician will 



THE NON-NEURONIC DISEASES 84/, 

serve his interests best by carefully guarding the family against any 
fallacious anticipations. If, however, consciousness partially or com- 
pletely returns, and the patient is a hemiplegic with or without aphasia, 
the physician can do a great deal, not only for the victim's comfort, 
but even to ameliorate to a large extent the distress caused by the 
various sequelae. In fact, this is the stage of apoplexy in which medical 
science can play its best hand. The storm has passed ; it now remains 
to restore order as far as possible out of the wreck, and in doing this 
the attendant can sometimes do wonders. In the first place, every 
precaution spoken of under the head of prophylaxis should be adopted 
to prevent a return of the shock. Absolute quiet, mental and physical, 
with the head elevated : light, nutritious, non-nitrogenous diet ; gentle 
sponging of the surface of the body ; abundance of fresh air ; and all 
those agencies calculated to cheer, invigorate and nourish the patient, 
so far as he is capable of being so acted upon, should be carefully 
thought of. 

While the clot is undergoing organization and surrounding itself 
Avith a capsule, the paralyzed muscles will become somewhat atrophied. 
To preserve the muscles in the hope of their resuming their function 
if the nervous centers should regain part of their power, faradism, 
massage and gentle passive movements are to be instituted. Just how 
soon this is to be done is the source of a difference of opinion. In my 
own experience I have found it advantageous to begin very early — 
gently, of course, at first — not later than the first or second week after 
the shock and subsidence of all signs of irritation or possible inflam- 
mation. Passive movements and the passage through the muscles of a 
current of faradic electricity, just sufficiently strong to produce easy, 
regular contractions, should be made systematically for a few minutes 
each day. I am fond of using olive or cocoanut oil when giving the 
massage, as it softens ,the skin and, I believe, favors to a slight extent 
the nutrition of the underlying tissues. At no time should anything 
cold be placed against the body, and at all times the patient should be 
clad with warm, non-irritating garments. Later on it is a good thing 
to encourage the patient to attempt voluntary movement. Of course. 
this will be impossible in many instances, but he should move the well 
side, and the attendant may assist him by raising at the same time the 
paralyzed limb. Ofttimes the patient thinks he is doing this of his 
own will, and the hopefulness which it inspires cannot but be of benefit : 
nay, more, such simple manoeuvres have kept the cortical memory or 
representative centers alive, so that when the motor areas had partially 
recovered their function the patient was better able to attempt and 
even succeed in performing voluntary movement than he otherwise 
would have been. Re-education of paralyzed, or rather partially 
paralvzed. muscles is an important part of the physician's duty. Many 
a hemiplegic would have been less hemiplegic if the memories of mus- 
cular movement had been preserved by the early practice of passive 
movement in conjunction with attempted voluntary movement. 

What I have just said applies likewise to the aphasia following the 
shock. The speech center should be encouraged to functionate, or at 
least an attempt made early in the trouble to awaken the activity "i" 



844 THE NON-NEURONIC DISEASES 

the corresponding speech center of the opposite side. These centers 
are memory or representative centers for speech, and hence if a patient 
is utterly neglected it will happen that when the center recovers from 
the shock, the power of speech will be much less than it otherwise 
would have been. Hence, as soon as consciousness is sufficiently re- 
stored, I have the nurse for a few moments each day teach, as she 
would a child, the names of persons and things, and if possible get the 
patient to repeat them after her. It is astonishing in a certain per- 
centage of cases how strikingly and rapidly the aphasic symptom may 
in part be recovered from by this prompt and regular re-education of 
the memory centers for speech. In cerebral as well as muscular physi- 
ology it is an axiom that exercise increases nutrition and function. 
Many an aphasic hemiplegic would undoubtedly have been less of an 
aphasic and less of a hemiplegic by the systematic exercise of his cere- 
bral structures as soon after the shock as possible, and when all signs 
of inflammation and irritation had subsided. 

In all traumatic cases, and in all cases in which the symptoms in- 
dicate a superficial location of the clot, trephining for the removal of 
the latter is to be taken into serious consideration. I recall the case 
of a boy of some five years of age who fell over a balustrade and sus- 
tained a severe concussion of the head, with the formation of an intra- 
cranial clot with all its accompanying signs of unconsciousness, local- 
ization and stertor. The spreading of the clot immediately after the 
fall could be clearly observed by the spreading and deepening of the 
muscular paralysis. Trephining was immediately performed, with a 
partial restoration to consciousness and a slight return of the muscu- 
lar power. The action of the muscles was a striking phenomenon. At 
first they were violently contracted, probably because of the irritative 
action of the clot ; then they became paralyzed completely, with a 
more or less set rigidity. After trephining they relaxed completely, 
and remained so, or were very feebly moved as a result of subcon- 
scious volition. Death occurred in a few hours, however, from ex- 
haustion and shock. The removal of a clot deep in the centrum ovale 
is a hazardous and difficult operation. It is attempted, however, but 
with little genuine success. The paralysis in such a case is not re- 
lieved, but a source of infection and irritation is removed and makes 
the operation at least one to be thoughtfully considered. 

I have very little faith in the so-called sorbefacient powers of such 
remedies as the iodide of potash, gold, arsenic, etc. As alteratives 
they may indeed somehow modify the clot or the results of its presence 
in the cerebral tissues, but I am inclined to chink that much of their 
effect is due to some kind of stimulant tonic power. At all events, their 
administration does seem to be of some benefit in some eases, and they 
are therefore to be commended. 



THE XOX- NEURONIC DISEASES 845 

ENCEPHALOMALACIA. 

EMBOLISM AND THROMBOSIS. 

Acute cerebral softening, or encephalomalacia, is a local anaemic 
necrobiosis caused by the sudden occlusion of an artery, and is char- 
acterized by an apoplectic stroke and hemiplegia. The immediate cause 
of the obstruction to the circulation is an embolus or a thrombus. The 
origin of the latter is an abnormal condition of the blood or vascular 
walls. 

Etiology. — The etiology of the circulator}' disease determines 
practically the etiology of encephalomalacia. Embolism generally oc- 
curs in the young and middle-aged, before the fortieth year. Throm- 
bosis is a complication of advanced years. Syphilitic thrombosis, how- 
ever, occurs in early adult life. Women are said to suffer more from 
embolism than men, but statistics differ on this point. 

The predisposing causes of both embolism and thrombosis are 
many and of the highest degree of importance. They are so clearly 
bound up with the pathology and pathogenesis of cerebral softening, 
that it will be well to discuss all together. 

Given the predisposing causes, certain exciting influences such as 
fright and other sudden mental shock, unwonted physical exercise. 
abnormal physiological strains of all sorts, parturition, sudden chilling 
of the skin, lowered heart action, etc., may provoke an apoplectic at- 
tack. 

Pathology and Pathogenesis. — Eighty-nine per cent, of the 
cases of embolism are associated with heart disease. Vegetations from 
acute or chronic endocarditis and segments from ulcerative processes 
within the heart are the source of the emboli. Heart clots in the 
auricular appendix and dvtring the puerperium have produced them. 
They may spring from a disintegrating thrombus elsewhere. Atheroma 
or aneurism of the aorta, as well as ulcerative bronchitis, disease in 
and about the pulmonary veins, and gangrene of the lung, 
may all be responsible for them. A history of rheumatism 
with valvular disease and cardiac weakness is present in the 
great majority of the cases of embolism. Changes in the condition 
of the blood itself wrought by such influences as the acute infectious 
fevers, pulmonary tuberculosis, puerperal sepsis and even anaemia have 
been credited with the formation of emboli. It is more likely, however, 
that an endocarditic condition is set Up under these conditions, which, 
together with the disturbed heart action, is the source of the clots. 
Such deteriorated blood states are more prone to originate thrombi. 
These, however, may send off secondary embolic particles, a view 
which is supported somewhat by the fact that in these infection- states 
the obstructions in the brain are usually minute and multiple. 

After reaching the brain an embolus usually lodges at the bifurca- 
tion of some vessel, or if small enough may pass on into an arteriole 
and completely occlude it. The middle cerebral artery and its end 
branches are the favorites. The left side is mostly affected because the 



846 THE NON-NEURONIC DISEASES 

blood current is most direct from the heart on that side. Other arteries 
may rarely be the seat of the obstruction. Emboli have gotten caught 
in the internal carotid, vertebral, deep cerebral and posterior cerebral 
arteries. 

Once lodged, the embolus becomes more or less closely attached 
to the vascular wall, at times calcified and the center of a secondary 
local thrombus. It may thus continue to grow and extend into the 
neighboring vessels. Sometimes it begins to break up and send off 
other emboli before necrobiosis has been instituted by the first. 

The thrombotic process is quite different from all this. Here 
syphilitic arteritis, senile atheroma, weakened heart action and various 
blood dyscrasise constitute the great predisposing causes. Alcohol, 
lead, gout, chlorosis, leukaemia and even heredity are obviously impor- 
tant elements in the causation of thrombosis in this manner. Multiple 
thrombi have been seen after extensive burns upon the skin and carbon 
monoxide poisoning. They may result secondarily, as I have already 
stated, from a fixed embolus. Oppenheim affirms that in his experi- 
ence atheroma has been incited by certain diseases of the nervous sys- 
tem and by continued emotional excitement in which there was a per- 
manent disturbance in the functions of the vascular apparatus. 

The most common location of a thrombus is the middle cerebral 
and basilar arteries, though it may start up anywhere. In a general 
way the base of the brain and the larger vessels are its favorite lo- 
calities. 

The complete occlusion of a vessel by an embolus or thrombus 
produces an intense local ancemia and if there is no anastomosis with 
other vessels, softening and destruction of tissue in the affected area. 
These softened areas may be found anywhere in the brain, most com- 
monly in the cortex and centrum ovale, where the blood vessels are of 
the terminal variety. The necrobiosis usually begins about a day and 
a half after the occlusion of the vessel, though swelling and other 
changes probably occur immediately. 

Red, yellow and white encephalomalacia are usually referred to by 
the pathologists. They are merely different stages of the necrobiotic 
process, the color being dependent upon the blood. Red softening is 
the first stage and is most marked in cortical foci. As the coloring 
matter of the blood changes in the affected area a yellowish hue is 
given to it. This is seen only after several weeks. Finally the yellow 
tinge passes into a white or bluish-white and the focus contains the 
debris of degenerated nerve cells and fibres. The presence of the 
myeline drops, parenchymatous detritus and granular cells aids in 
distinguishing this condition from mere post-mortem maceration. 
Absorption ultimately takes place, a cyst is formed, contracts and leaves 
a permanent cicatrix. Inflammation, suppuration and sclerosis may all 
be observed in the affected and adjoining areas. The size of the 
softened focus may he from that of a pinhead to an entire hemisphere. 
It may be large and single or small and multiple. 

It is unnecessary to describe here the contributory pathological 
findings in encephalomalacia, such as the diseases of the heart, blood 
vessels and other organs. 



THE NON-NEURONIC DISEASES 847 

Symptoms. — The onset of embolism is usually sudden and without 
premonitory indications. In rare cases there may be the slightest sort 
of paresthesia immediately before the occlusion, especially if the 
embolus should catch at a bifurcation. If the obstructed artery is 
particularly small there may be no disturbance of the consciousness. 
Usually, however, after some local or general convulsive twitchings, 
hemiplegia appears and then temporary loss of consciousness. The 
coma is lighter and of shorter duration than it is in hemorrhage. The 
temperature does not alter at first, but in a few days it rises somewhat. 
In septic embolism it may attain a very high degree and be preceded 
by distinct chills. A unilateral epiletiform seizure, or even a condition 
resembling status epilepticus, may take the place of the coma. In 
some cases merely drowsiness with slight delirium occurs. Vomiting, 
flushed countenance, stertorous breathing and other symptoms of hem- 
orrhage are wanting. The pulse is feeble as a rule, the countenance 
slightly paler than normal and the skin cool. 

Thrombosis is always preceded by prodromes. These are so in- 
sidious, varied and prolonged sometimes that mistakes in diagnosis are 
easily made. In syphilitic cases they consist of headache, queer feel- 
ings about the body, temporary attacks of double vision, cranial nerve 
palsies and sudden spells of weakness. In other cases hysteroid mani- 
festations may be observed ; vertigo, extreme emotionalism and irrita- 
bility, numbness of the hands and feet, temporary aphasia, transient 
hemiplegic attacks and periods of drowsiness and stupor. Loss of 
memory, incoherence of speech, slight dysarthria, temporary attacks 
of disturbed respiration and heart action add to the confusion. Swal- 
lowing may be troublesome at times, a slight cough may appear and 
other temporary symptoms may indicate bulbar difficulty. When the 
attack begins in thrombosis the loss of consciousness is gradual. If 
the vessels involved are small, or it is due to syphilis, there may be no 
disturbance of the mind ^whatever. The hemiplegia is usually slow- 
in developing and precedes somewhat the development of the coma. 
Neither the paralysis nor the loss of consciousness is as deep as it is 
in hemorrhage, nor as abrupt and limited as it is in embolism. The 
hemiplegia is variable and rarely complete. The temperature may tall 
slightly in the beginning just as it does in hemorrhage. As the basal 
arteries, such as the basilar, vertebral and posterior cerebral, are more 
liable to be the seat of thrombosis than of hemorrhage, basal and 
bulbar manifestations are to be expected more in the former. 

The hemiplegia of both embolism and thrombosis tends toward 
rapid and early improvement, unless a very large vessel has been ob- 
structed. It may be preceded for some days by a hemiparesis-, but as 
a rule it appears pretty much in the same way that it appears in 
hemorrhage. If it is right-sided, aphasia accompanies it. 

The conditions after the subsidence of the acute stage are tin- same 
in softening as they are in hemorrhage. Occasionally, however, in 
cortical softening the limitation of the area affected gives rise to 
limited paralyses, monoplegias, aphasia alone or monoplegias with 
hemianopsia. Hemianaesthesia may appear with the hemiplegia or 
exist alone. 



848 THE NON-NEURONIC DISEASES 

The location of the softened spot cannot always be determined 
from the clinical picture, for the lesion may be a multiple one. In many 
cases, however, the vessel occluded and the area involved can be more 
than suspected from the peculiar character and grouping of the symp- 
toms. One needs only to recall the functions of the particular part 
of the cortex supplied by the affected artery. 

Bulbar and pontile symptoms occur when the vertebrals or basilar 
artery is obstructed. In the case of the former the symptoms are 
those of acute bulbar paralysis, as detailed elsewhere. „ In the latter 
the paralysis is apt to be bilateral, associated with rigidity or spasm, 
and accompanied by a rapid rise of temperature. 

The results of obstruction in the internal carotid are very variable 
on account of the anastomoses in the circle of Willis. If these are 
abundant, the vessel may be ligated and no paralysis will follow ; if the 
vessels are too narrow or wanting, the softening may be very extensive 
with hemiplegia, permanent coma and early death. In such a case 
the clot usually extends into the branching arteries. The inclusion of 
the arteria centralis retinae in this same lesion provokes of course most 
serious visual disturbances. 

Of all the arteries the middle cerebral is the one most commonly 
affected. The internal capsule is softened and a permanent hemiplegia 
is established, with temporary or permanent hemianesthesia. Aphasia 
occurs with disease of the left artery. If one of the branches of the 
artery is obstructed, the symptoms will follow the localization of the 
encephalomalacia in the particular convolutions supplied by those re- 
spective branches. Hence various monoplegias, hemiplegia and motor 
aphasia will develop. Facio-lmgual monoplegia follows obliteration of 
the first branch, and aphasia also, if it is on the left side. The second 
branch when occluded causes a facio-lingual paralysis. The third and 
fourth branches supply the lower part of the parietal lobes, including 
the supra-marginal and angular gyri. Their damage results in alexia, 
in hemianopsia and zvord-deafness. When the fifth branch is plugged 
word-deafness is the main symptom. 

It will be noted that our modern knowledge of cerebral localiza- 
tions, coupled with the knowledge of the minute circulation of the 
brain, underlies our appreciation of these various groups of symptoms. 

The anterior cerebral arteries supply the anterior parts of the brain. 
Their obstruction is compensated for in part by the middle cerebrals. 
No symptoms therefore usually occur, though it has been thought that 
mental inefficiency as well as monoplegia of the leg have been caused 
by it. 

Diagnosis. — The most important, and ofttimes the most difficult, 
differential diagnosis to make is between hemorrhage and acute soft- 
ening: The subject is discussed under the head of cerebral hem- 
orrhage, but it will probably be well to enumerate here some of the 
more significant differential signs. In acute softening early and late 
period of life point respectively to embolism and thrombosis. Hem- 
orrhage occurs more particularly in the latter half of adult life and at 
the beginning of old age, from forty to sixty approximately. In acute 
softening there is a history of syphilis, rheumatism with recurrent 



THE NON-NEURONIC DISEASES 849 

endocarditis, infection or an atheromatous condition of the arteries ; 
in hemorrhage heredity and vascular disease are present somewhat. 
Abrupt onset without premonitory indications, sudden deep coma, gen- 
eral paralysis that shows a tendency to recede and become more re- 
stricted in its distribution, unequal pupils, conjugate deviation of the 
head and eyes, flushed face, full bounding pulse and the temperature 
phenomenon indicate hemorrhage ; whereas in acute encephalomalacia 
prodromes are frequent, much more so in thrombosis than in embolism, 
the paralysis and loss of consciousness approach more gradually, the 
former slightly preceding the latter, the limbs are convulsed, the heart 
is weak, the muscles are not completely relaxed, and the temperature 
phenomenon of hemorrhage is absent. Aphasia is common in embol- 
ism, as the lesion usually affects the left side ; and mental changes 
characterize thrombosis on account of the prolonged disturbance of 
the nutrition of the brain. 

Prognosis. — The prognosis in regard to life is generally favor- 
able in softening and as compared with that of hemorrhage during the 
stage of coma the hope of recovery may be expressed with a greater 
degree of positiveness. However, it is an unfavorable sign if the 
coma is deep, the heart action bad and the patient does not come to 
for several days. 

The outlook in carotid and basilar thrombosis is bad. . Recovery 
practically never takes place, though the end may be long deferred, 
the patient continuing sometimes for months and even years, experi- 
encing remissions and relapses in thrombosis particularly. I have seen 
several of these cases variously diagnosed and treated by different 
practitioners during a period of many months, in one case over a year. 

Recurrence is less prone to appear in embolism than in thrombosis. 
Most of the heiniplegics that continue to live many years without a 
relapse owe their paralysis to a small area of softening. 

In regard to the future outlook for the hemiplegia, it is about the 
same in softening as it is in hemorrhage. If after the first month 
there is no change, the patient had better be informed of the perma- 
nency of the condition. Speech disturbances are apt to be a little more 
fixed here than in hemorrhage after a certain period has been passed, 
and yet in the latter the initial aphasia usually lasts a trifle longer. 

In arriving at the prognosis of encephalomalacia the extent of the 
lesion and the location of the obstruction exercise great weight. 

Treatment. — The differential treatment of the comatose stage 
of acute softening, and the general management of the sequelae, are dis- 
cussed in detail under the head of cerebral hemorrhage. I desire heir 
merely to reiterate the injunction to do as little as possible, in >< •un- 
cases practically nothing, until it is decided whether tin- case is one of 
softening or hemorrhage. If it is the former, the patient had l» 
be placed horizontal or even with the foot of tin- bed slightly elevated. 
As the clot cannot be removed, it is desirable to urge it on to a smaller 
vessel if possible and to fix it there as soon as possible. Its furthci 
enlargement is to be prevented by every means in our power. Tin 
indications for the accomplishment of these ends are t<> favor the 
flow of the blood towards the head by gravity and stimulation of the 



850 THE NON-NEURONIC DISEASES 

heart and by avoiding ail measures that have a tendency to deplete the 
blood. Venesection must be rigidly avoided. The bowels must not 
be acted upon with cathartics too soon. The patient must be kept 
at absolute rest with his head low. Alcohol, digitalis, strophanthus, 
strychnia and nitroglycerin are available for stimulating the circula- 
tion. With these exceptions, the treatment of apoplexy from arterial 
obstruction differs in nowise from that of apoplexy from hemorrhage. 

A history of syphilis calls for the prompt administration of mer- 
cury and the iodides. These had better be continued for a long time 
with the heart stimulants and general tonics. 

The management of the hemiplegia, aphasia and other symp- 
tomatic treatment are discussed elsewhere. 

THROMBOSIS OF THE INTRACRANIAL VEINS AND 

SINUSES. 

Thrombi are liable to form in any of the intracranial veins and 
sinuses. They are of serious import both on account of the effects 
they themselves produce, and on account of the effects produced by the 
malady of which they are a collateral result. 

Etiology.— Etiologically, thrombi must be divided into the pri- 
mary and secondary. A primary thrombus is one that forms merely 
on account of the inherent state of the blood or the circulation. A 
secondary thrombus is the outgrowth of some serious disease, usually 
septic, in the neighborhood. 

Primary thromboses are called "marantic," because they usually 
occur in adynamic states. Children and the aged are usually affected, 
though, of course, all ages are subject to marantic conditions or states 
of marasmus. In exhausting diarrhoeas, such as infants particularly 
suffer from, wasting pulmonary affections, prolonged fevers and long- 
continued suppurative processes, even acute specific maladies, the 
blood is so altered and the heart is so weakened that coagulation readily 
supervenes in these veins, where the circulation at best is not an active 
one. The anatomical structure of a sinus precludes any great elas- 
ticity in its walls ; hence when the blood is thinned and diminished in 
amount in these low states, the sinus does not contract and equalize 
the circulation. This fosters stasis and coagulation. Anaemia less 
frequently than chlorosis provokes a primary thrombosis. Severe hem- 
orrhages have been followed by it. It occurs in adults sometimes after 
a long cachexia, such as cancer and phthisis. The puerperal state 
must at times be charged with it. 

The superior longitudinal sinus seems to be the favorite site tor 
the formation of a primary thrombus. After this come the lateral and 
cavernous sinuses. There are certain mechanical features about the 
circulation that go far towards explaining this selective action on the 
part of the clot. The collateral veins that enter the longitudinal sinus 
do so at an angle and in a direction the reverse of that of the blood 
current in it. The sinus and venous currents thus meet in opposing 
directions. The latter also have to ascend to reach the main flow in 
the sinus besides themselves receiving blood from ascending arteries. 



THE NON-NEURONIC DISEASES §5 1 

The irregularity of the inner wall of the vessels has some effect also, 
as is shown by the fact that the clot is attached, as it were, to one side 
while the blood goes flowing along in the channel beside it. 

Secondary thrombosis is usually the product of a phlebitis in the 
sinus wall or of the veins entering it. This phlebitis is most commonly 
originated by caries of the bone or internal ear disease. It is the 
result of a septic process generally of infectious origin. Nearly every 
sinus is the recipient of veins from the exterior of the skull. The 
transverse sinus receives thus through the mastoid foramen a vein 
which brings in blood from the occipital and posterior auricular veins 
on the outside of the head; while the longitudinal sinus receives a 
communication through the parietal foramen from the external veins 
of the skull. Other sinuses are similarly supplied. 

Injuries to the bone with inflammation of the diploe, tubercular 
meningitis, erysipelas, carbuncle of the face or neck, malignant ulcera- 
tion, orbital phlegmon, panophthalmitis and suppurating eczema of the 
scalp are all sources of the infection. A general septicaemia is to blame 
for it sometimes. Compression of the sinus has been followed by a 
secondary thrombosis. 

Of course, these secondary thrombi always occur in the sinus that 
is nearest to the primary seat of infection. The ear is probably the 
most common seat and hence these thrombi are most frequently seen 
in the superior petrosal or lateral sinus. Unlike the primary thrombi, 
they are rather infrequent in the superior longitudinal sinus. 

Pathology and Pathogenesis. — All or part of a sinus may be 
filled with the clot. In rare instances every sinus has been the seat 
of the thrombotic formation. The clot is dark red, soft and friable 
if recent, but is lighter in color, harder, more friable, granular and 
laminated if an old one. Recent clots are not quite as adherent to the 
sinus wall as are the older ones. Secondary thrombi are usually asso- 
ciated with phlebitis, are puriform and softened. The veins are not, 
as a rule, inflamed in the primary or marantic thrombi. It is said that 
Heubner recovered microorganisms from what seemed to be primary 
thrombi. In secondary thrombi abscesses are observed in the vessel 
walls, and masses of pus are discovered in even remote veins, such as 
the subclavian and superior vena cava. Meningitis is common under 
these conditions, naturally. 

Behind the thrombus there is, of course, congestion, oedema. The 
contributing vessels are engorged and swollen. The capillaries arc 
often ruptured in the gray substance of the brain and there arc in- 
numerable, minute hemorrhagic foci. 

A sinus thrombus may be compensated for by the blood passing 
around by another channel. This is not possible in venous thromb >sis. 
The veins not encasing the clot are tortuous and dilated. 

Softening occurs in the cerebral tissues as a result of the oedema 
and hemorrhage. Tt may be very extensive or minute or in innumer- 
able scattered or mulberry-like spots. Meningeal hemorrhage takes 
place occasionally, but rarely. 

If recovery should happily take place, the damage is liardh as 
great as that which is left after arterial obstruction. Secondary 



852 THE NON-NEURONIC DISEASES 

abscesses have been found in the lungs and remoter parts |fcom a soft- 
ened, scattered intracranial thrombus. Gowers says that in about half 
of the cases of secondary thrombosis these secondary remote septic 
abscesses are found. 

Symptoms. — These are not very distinctive. They are very apt 
to be masked by the symptoms of the disease out of which the throm- 
bus originated. In primary thrombosis, for instance, the adynamia, 
the anaemia, the heart weakness, the chlorosis are so prominent that one 
loses sight of the symptoms caused by the sinus obstruction. The ear 
disease, the meningitis, the septic manifestations generally quite over- 
ride the signs of the secondary thrombus that may be present. 

The presence of an obstruction to the venous flow in the brain 
would be expected to produce two sets of symptoms — namely, those 
of a local character depending upon the location of the clot and the 
part of the brain implicated, and those dependent upon the disturbed 
circulation outside of the head. Neither of these, however, are at all 
characteristic, and the latter, which are the most so, are at the same 
time the rarest. A clot in the sinus produces obvious enough mani- 
festations in the external cranial and facial veins that happen to pass 
through and connect with that sinus ; but unfortunately the phenomena 
are not often to be seen. 

Superior Longitudinal Sinus. — Thrombosis of this sinus may be 
accompanied by an cedematous condition in the cranium and a dilated, 
twisted and tortuous state of the veins lying over the frontal, parietal 
and temporal bones. Venous epistaxis may occur from the vessels of 
the nose that connect with it in front. In children, who have been 
afflicted with exhausting diarrhoea, the fontanelles are usually de- 
pressed. When this thrombus appears, however, the fontanelles bulge 
and become very tense from the associated oedema and congestion. 

Among the cerebral complications are to be noted symptoms simi- 
lar to those of increased intracranial pressure, meningitis and soften- 
ing. There is apathy, stupor, somnolence, even coma. Severe head- 
ache is indicated, with vomiting and convulsions. Delirium is some- 
times present. The convulsions may be local or general. Rigidity of 
the neck and back, as in opisthotonos, more or less obtains. Tremor, 
incoordination and 'Contracture, strabismus and paralysis of the limbs 
are possible symptoms. The paralysis may be unilateral if the clot 
extends into the veins covering one hemisphere. Even monoplegic 
phenomena have been rarely seen. Aphasia is almost unknown. 
Hemianaesthesia has been but infrequently observed. 

The pulse and respiration are variable. They may be normal or 
subnormal. They are usually elevated near death, which in most 
patients occurs in coma in a few days or a week or two. The tempera- 
ture as a rule is normal, though it has risen in leaps at times, even as 
high as 108 degrees F. 

These symptoms are so irregular and indefinite that it is clear a 
diagnosis can only be made upon the etiology and signs of congestion. 
Often no diagnosis can he made, for a similar clinical picture can 
occasionally be presented by infantile hydrocephaloid disease, chloro 
meningitis, encephalitis and cerebral hemorrhage. 



THE NON-NEURONIC DISEASES 853 

Cavernous Sinus. — Here the eyelids and temples are apt to be 
cedematous, and the veins in and about the orbit to be tortuous and 
dilated. The eyeball may be protruded and the optic papilla (edematous. 
It is said that even choked disc has been observed. The retinal veins 
have certainly been congested. Amblyopia and amaurosis have result- 
ed in some cases, even with a normal appearance of the eye ground. 
Neuralgic pains have been felt in the fifth nerve and headache is 
common. The nerves that run to the orbit in the wall of the sinus, such 
as the third, fourth and sixth nerves, are liable to be involved. Neuro- 
paralytic manifestations may be not unexpected. 

Petrosal Sinus. — There are no known symptoms of thrombosis in 
either of the petrosal sinuses. 

Lateral or Transverse Sinus. — There is here apt to be oedema 
behind and over the mastoid process. Gerhardt's observation is open 
to question — namely, that the external jugular vein on the affected 
side is less full of blood than it is on the unaffected side, because on 
the affected side of the head the blood that should flow into the external 
jugular flows largely on account of the presence of the clot now into 
the internal jugular. There are no distinctive cerebral symptoms, but 
there have been observed disorders of the ninth, tenth, eleventh and 
twelfth cranial nerves. 

In secondary, phlebitic thrombosis there is not much direct dam- 
age done to the brain. The meningitis that is present, however, may 
provoke marked cerebral manifestations and the septic source of the 
whole trouble may lead to a cerebral abscess. The mere occlusion, 
however, does not produce these or other distinctive cerebral phenom- 
ena. Sometimes the clot itself is the seat of a violent purulent process. 
It softens and breaks down and lights up a virulent form of septicaemia, 
with the establishment of secondary distant foci in the lungs and else- 
where, these being the first indications of the presence of the clot. 
These secondary septic symptoms are of the usual character and need 
no special description here. 

Among the cerebral symptoms that now begin to appear are to be 
noted apathy, dullness, stupor, headache, motor and sensory irritative 
meningitic phenomena, such as unequal paralysis, muscular twitchings, 
rigidity and disordered sensation. These secondary thrombi last from 
a few days to a couple of weeks and the sufferer dies in coma. Rec 
ery is so rare as hardly ever to be counted upon. Primary clots offer 
a better prognosis, sometimes being absorbed entirely or leaving per- 
manent cerebral damage. 

Prognosis. — This is very serious in all eases. Secondary phlebitic 
thrombosis is practically a fatal disease. ( )ccasionallv in children the 
symptoms of a primary, marantic clot disappear. In adults this is much 
rarer. If the general signs pass away, there may nevertheless remain 
some local permanent damage and disorder. I Operative treatment has 
improved somewhat the prognosis of the secondary thrombi. The 
secondary results, such as the leptomeningitis, cerebral ab ptic 

foci in the lungs, have their own prognosis, which, of course, deter 
mines that of the thrombosis. 

TREATMENT. — The treatment of sinus thrombosis almost limits 



854 THE XOX-XEUROXIC DISEASES 

itself to the treatment of the cause. In the primary form the vigor and 
general health must be restored as rapidly as possible. The circulation 
should be stimulated and tonics administered. Never should blood- 
letting be practiced. The recumbent attitude with the head slightly 
elevated should be maintained and flexion of the neck must be care- 
fully avoided. 

In the secondary form all accessible foci of pus should be sur- 
gically drained. The statistics of some surgeons are remarkably favor- 
able. According to Henschen, of 145 cases, fifty-eight per cent, were 
cured. The reader is referred to works upon surgery for further 
details. When septicaemia is general, tincture of the perchloride of 
iron, quinine and the salicylates should be persistently administered. 

INFANTILE HEMIPLEGIA. 

The cerebral palsies of childhood constitute a group of cases that 
has provoked hitherto a great deal of discussion and much unnecessary 
refinement of classification. As the name indicates, and as will appear 
in the study of their pathology and pathogenesis, they are all due pri- 
marily to some defect or lesion in the brain. They are all hemiplegic 
in character and distribution. If the lesion extends to bilateral parts of 
the brain, the hemiplegia is bilateral or double, and the disease is known 
as cerebral diplegia. No distinction of any practical value can be 
made between unilateral and bilateral hemiplegia in childhood except 
upon an etiological and pathological basis. As no such basis is yet 
known, we must perforce continue to recognize them both as mani- 
festations of the same general trouble. 

Under the name of Little's disease, cerebral paraplegia, congenital 
or juvenile spastic paraparesis, congenital spastic rigidity of the limbs, 
some writers have endeavored to establish a separate affection, though 
they admit that it is cerebral in origin, in the vast majority of cases at 
least, and that the paralysis has all the characteristics of a true hemi- 
plegia. The term paraplegia, which has become so fixed as a defini- 
tion of spinal paralysis, is extremely inappropriate. The limitation of 
the palsy more particularly to the lower limbs, the absence of certain 
mental manifestations, and the prominence of the lesion in the pyra- 
midal tracts do not in the least withdraw Little's disease from the 
double hemiplegias of childhood. On the other hand, the etiology, 
pathogenesis and symptomatology show very conclusively that it is 
primarily cerebral in origin with secondary changes in the cord char- 
acteristic of all hemiplegias. 

All of the cerebral palsies of childhood now under consideration, 
including Little's type, are due to a degenerative change in the upper 
motor or cortico-spinal tract. The unilateral or bilateral distribution of 
this degeneration is a mere matter of etiology. By all the more recent 
pathologists it is believed that cortical disease of some sort is to he 
charged with the beginning of the degeneration. The separation of 
these palsies into different types therefore merely on account of the 
distribution of the paralysis, their relationship to the act of parturition, 
or the prominence of the lesion in the pyramidal tracts is unnecessary, 



THE NON-NEURONIC DISEASES 855 

unwarranted and confusing. The only way to dispose of them, until 
we have a better foundation for differentiation than we have to-day in 
their etiology and pathology, is to group them all together in a single 
class and to discuss them under the head of diseases of the brain or of 
the upper motor segment. 

Etiology. — The cerebral palsies of childhood are accidental and 
are therefore not influenced by such etiological factors as heredity, 
age, sex, nationality, climate, etc. Their causes are numerous ; for 
the sake of convenience, therefore, we divide them into the prenatal, 
natal and postnatal, remembering all the while that the same immediate 
cause, as, for example, cerebral hemorrhage or embolism, may be the 
same in all three periods. 

In about one-third of these palsies the cause is prenatal, and we 
denominate the disease congenital. The damage to the brain is ac- 
complished during intrauterine life and the disease is merely congenital 
and not in the least hereditary, as I have seen it stated. Intrauterine 
traumata,, injuries to the mother during pregnancy, psychic shocks. 
any accident in fact that may cause an inflammation to the motor zone 
of the fetal brain, are among the more common prenatal causes. 
Hemorrhage and embolism are the lesions in the majority of these 
cases. Hereditary syphilis has been credited with the disease, though 
this is open to doubt. The evidences of a meningoencephalitis, which 
Striimpell believed to be the underlying condition in the diplegic cases, 
are not forthcoming, though it is still held that syphilis and other toxic 
influences are at work in some cases. Simple agenesis, or lack of brain 
development, ab initio, without apparent cause, traumatic or toxic, may 
account for a few cases. 

The cases due to injury during birth are more numerous. Among 
these natal causes should be remembered slow and tedious parturition, 
compression of the head by tjie mother's birth passage or by the for- 
ceps, retention of the head high up before delivery, precipitate labor, 
etc. Most of these accidents occur in first labors and many of them 
are associated with asphyxia and foot presentations. The possible 
existence of a prenatal cause should always make one hesitate before 
positively attributing the accident to one of these obstetrical causes. 
The most skillful use of the forceps will not save an obstetrician's rep- 
utation if the child is paralyzed, though from an almost positively es- 
tablished prenatal accident. The laity have unfortunatel) acquired the 
notion that all these forms of paralysis arc due to the use of the 
forceps, and it behooves us to re-educate them. In these eases the 
lesion is usually thrombosis, embolism, meningeal or intracerebral 
hemorrhage. They are less frequently diplegic in character than are 
the prenatal cases, and they are more distinctively hemiplegic. 

The postnatal cases may be hemorrhagic and due to traumata, bill 
they are more commonly due to disease, tumor and general c institu- 
tional influences. It is these cases thai Striimpell believed especially to 
be dependent upon a polioencephalitis, an affection analogous to and in 
the same general category as poliomyelitis, [nfection certainly plays 
here a large role; measles and scarlet fever with nephritis and endo 
carditis cspeciallv being frequent among its antecedents, h lias h-m 






856 THE NON-NEURONIC DISEASES 

attributed also to pneumonia, pertussis, variola and even vaccination. 
Vascular disease and probably embolism are the immediate causes of 
the paralytic condition. Cranial injuries and mental shock in pro- 
voking hemorrhage are undoubtedly among the later postnatal causes. 
In one case the child was thought to be dead immediately after birth 
and allowed to lie a long time exposed upon a marble slab. It is 
doubtful, however, whether the disease is ever produced in this way, 
especially in the absence of infection or trauma. 

Pathology and Pathogenesis. — The pathological findings in the 
cerebral palsies of infants are numerous and varied. In one thing only 
are they uniform, and that is in their involvement of the cortex and 
related subcortical and spinal structures. The varied etiology of the 
trouble causes the varied pathology. The relationship of the clinical 
picture to the morbid anatomy is not always as distinct as could be^ 
desired, but the connection between the primary cortical damage and 
the secondary spinal degeneration is definitely recognized. Post- 
mortem testimony affirms very clearly that the pathogenesis of all this 
class of paralysis involves a simple agenesis, or failure of brain develop- 
ment, a general diffuse sclerosis of the cortex following, perhaps, a 
meningo-encephalitis or a very doubtful polioencephalitis, a hemorrhage 
or an encephalomalacia from embolism or thrombosis. These condi- 
tions do not differ per se from the same conditions in the adult ; but 
as they occur in the young and undeveloped brain, their ultimate re- 
sults are not the same. An inflammation, sclerosis or a compressing 
clot that prevents the growth of the brain will, of course, produce a 
different pathological and clinical exhibition from that produced by the 
same influences in a fully grown brain. The same is to be said of the 
secondary degenerations in the underlying related tracts. The most 
obvious of the congenital changes thus brought about is the condition 
known as porencephaly. In all of these conditions the motor area of 
the cortex is almost constantly involved. In rare instances it may be 
the only area implicated. In the larger number of cases other parts of 
the brain are also affected, though, it may be, not so obtrusively as the 
motor areas. The general process is a more or less diffuse one, with 
the initial focus usually in or near the motor elements, but occasionally 
away from them. Thus porencephaly as well as other changes have 
been found in the occipital lobe and cerebellum, with corresponding 
congenital clinical manifestations. On account of the porencephaly, 
late sclerosis with induration and atrophy of the hemispheres, it is 
often quite impossible to make a satisfactory guess as to the exact 
nature of the original lesion or disorder. 

Many cases are believed to be due to simple failure of development. 
cerebral agenesis, without any other discoverable cause or pathogenetic 
factor. The nervous elements in the cortex exhibit microscopic changes 
that suggest mere defective development. Such cases have been 
studied especially by Sachs and may in part explain such anomalous 
observations as that of ( )ppenheim, wherein a mother and a daughter 
were afflicted with the same type of paralysis. 

A general, diffuse sclerotic condition of the cortex is found more 
frequently than that of simple agenesis. This is probably due to a 



THE NON-NEURONIC DISEASES 857 

low grade of chronic inflammation, which may have been chronic from 
the beginning or have succeeded a meningoencephalitis. If the in- 
flammation is more or less localized, it may have diffused itself from 
a focus started by a hemorrhage or other trauma ; or if it is so 
widely spread out as to involve the greater part of the cortex it is 
probably toxic or infectious in origin. The few cases that are attribut- 
ed to syphilis, and the many that seem to follow the infectious fevers, 
may thus be explained. A whole hemisphere may be affected thus, and 
on account of the atrophy may be rendered much smaller than it nor- 
mally should be. This is sometimes called lobar sclerosis. Excrescences 
in the brain substance, hypertrophic sclerosis and hydrocephalus are 
accompaniments sometimes of this condition. The effort of Strumpell 
to align these cases, in part at least, with infantile spinal palsy by at- 
tributing them to a pure polioencephalitis, has not been very successful ; 
largely because no evidences of such inflammation, apart from men- 
ingo-encephalitis, have been found post mortem. The hypothesis, how- 
ever, is not unworthy of further investigation. 

By all odds the great majority of these cases, even of the diplegic 
type, are due to hemorrhage, embolism or thrombosis. The relative 
frequency of these respectively cannot be definitely determined. In 
traumatic cases, whether intra- or extra-uterine, intra-cerebral hem- 
orrhage certainly accounts for the hemiplegia, while meningeal hem- 
orrhage explains the bilateral or diplegic paralyses. Infective and toxic 
states, with the associated vascular disease, are the general causes 
underlying most of the cases of embolism and thrombosis. Areas of 
focal softening, dried-up cysts and spots of cicatricial atrophy are the 
evidences usually presented. 

When the nutrition of a part of the brain is shut off by direct 
damage or by arterial obstruction, it ceases to grow, a large cavity 
is formed, which may extendi into the ventricle, funnel-shaped and the 
condition of porencephaly established. This is usually prenatal in 
origin, though it may start after birth. It is said to occur in about one- 
fourth of the cases. It may be observed in one or both hemispheres. 

A curious condition that has been found in the brains of some of 
these diplegics is that known as microgyria. It is a developmental 
anomaly clearly and reveals a great increase in the number (A gyri 
and intervening small sulci. The whole gray cortex seems to be fold- 
ed in and out much as it is in the vermis cerebelli. < >tto has illustrated 
it well. 

The secondary changes in the projection tracts from the defective 
cortex are again slightly different from what they are in the adult 
cases. The development is checked and not fully developed elements 
merely destroyed. Some have thought that this developmental inhibi- 
tion might be primary in the cord and s. 1 accounl for the rases of 
supposed primary congenital spastic paraplegia. This is very doubtful. 
however. Developmental degeneration in neuraxones withpul primary 
changes of any sort in the related cell bodies would upset all our mod- 
ern ideas in regard to neurone histopathology. 

Symptoms. — In most of the cases of infantile cerebral palsy tlu- 
disease does not attract attention until the paralysis i- quite noticeable. 



858 THE NON-NEURONIC DISEASES 

Only in the postnatal cases can the initial phenomena be observed, and 
even in these cases they are frequently overlooked or misinterpreted. 
According to the nature of the case, they consist of a unilateral or 
general convulsion, followed by a hemiplegia, or a febrile outbreak 
with vomiting, delirium, stupor, followed by a more or less diplegic 
form of paralysis. Instead of one or two general or unilateral con- 
vulsions, a series of spasms may appear for several days or weeks, and 
ultimately pass into a state of bilateral or unilateral hemiplegia. The 
convulsions may occur at or immediately after birth, but the paralysis 
may not be noticed for weeks or months later. This is not so much 
due to the fact that the paralytic is far removed from the convulsive 
stage as that the former is not made obvious until the period has ar- 
rived at which the finer movements of the limbs, which suffer the 
most, would normally begin to announce themselves. Therefore most 
of the cases of cerebral palsy in children occur in the period between 
six months and three years of age. The infantile peculiarities of these 
hemiplegias are due obviously to the fact that they occur in the 
preeminently developmental period of life. 

The two prominent features that stand out in the clinical picture of 
these palsies are the characteristic paralysis of the extremities and cer- 
tain other symptoms that are even more distinctively of cerebral 
origin, such as epilepsy, strabismus, speech troubles and psychical dis- 
turbances. 

The paralysis in the limbs, as I have said, follows soon after the 
convulsive stage. It is distinctly a hemiplegia or unilateral symptom. 
It usually involves the lower extremities more than the upper. In some 
cases its onset is the same as it is in the hemiplegia of adults. The 
entire body is convulsed and paralyzed during a brief comatose stage. 
Gradually, however, one side of the body recovers leaving the face, 
arm and leg of the opposite side limp or immovable. More frequently 
spasmodic movements occur in the face, eyes, neck, arm or leg. As 
these quiet down, some slight return of movement appears in the face, 
then the arm and even the leg. The face as a rule quickly regains its 
normal appearance and activity ; the arm continues to improve until 
in some cases it may appear to be quite natural again ; the leg, how- 
ever, usually recovers only in part and is nearly always permanently 
affected. When the arm continues to be paralyzed the leg as a rule 
is still more so. When the age arrives for the child to attempt walk- 
ing, the paralysis of the limbs becomes extremely obvious and often it 
is not until this time that the parents fully realize that their child is 
seriously affected. The attempted steps taken by the little one arc 
seen to be awkward, difficult, stiff and jerky. In the course of time 
the gait assumes a. characteristic manner. The strong adduction of 
the legs, their irregular, stiff, spasmodic movements and their want 
of equilibrium in the activity of the antagonistic sets of muscles, cause 
the typical cross-legged progression and attitude shown in the accom- 
panying photographs. The knees rub against each other, the joints 
are slightly flexed, and the foot is so extended that it rests entirely on 
the balls of the toes. Rigidity, motor weakness and marked exagger- 
ation of the knee-jerks can all be observed. There are no sensory 



THE NON-NEURONIC DISEASES 



859 




O 






^ ■= 











86o THE NON-NEURONIC DISEASES 

symptoms, no muscular atrophy, or very little, no electrical alterations 
of importance ; simply a spastic, motor paralysis with contracture in 
certain groups of muscles resulting in a characteristic gait and attitude. 

The arms may or may not be affected in company with the legs_ 
When they are, their movements and attitude are typical. As they are 
less involved as a rule than the legs, their movements are not so rigid 
and weak as they are choreic and athetoid or vermicular and waxy-like. 
The joints are somewhat flexed and the muscles contractured. Ad- 
duction, flexion and exaggerated tendon reflexes are characteristic- 
phenomena. 

I have described the above symptoms as being hemiplegic in order 
to impress the fact that they are unilateral in origin. As a matter of 
fact they are bilateral in distribution, and being more frequent and more 
marked in the lower than in the upper extremities, the entire clinical 
picture so closely resembles a spinal paraplegia that it affords some 
slight ground for the suspicion that there may be a primary spastic 
paraplegia in infants comparable to the adult primary spastic para- 
plegia of Erb. Until the existence of spinal spastic paraplegia is better 
established than it is to-day, it seems to me preferable to apply to these 
cases the name diplegia, or double hemiplegia, and not the misleading 
term paraplegia. 

In the cases that are distinctively unilateral the same general de- 
scription of the paralysis applies, except that here the arm is more 
affected than the leg. The face usually manifests irritative rather than 
paralytic symptoms. The tongue is temporarily involved. The leg- 
recovers earlier and more than the arm. In a word, the clinical pic- 
ture is identical with that of cerebral hemorrhage, embolism and throm- 
bosis in adults. The motor weakness, the rigidity, the flexions, the 
contractures and the exaggerated reflexes differ in nowise from the 
adult forms, only as they interfere with the further development of the 
parts. Deformity, shortening, diminution in size and muscular wasting' 
from non-use are the inevitable results. All degrees of the trouble may 
be observed, from a scarcely perceptible rigidity up to an extreme 
paralysis. The tendon reflexes are always increased and the muscular 
tone heightened. Occasionally an ankle clonus may be evoked. The 
arm may be paralyzed and the leg merely spastic. In fact, great varia- 
bility occurs in the grouping of the symptoms of infantile hemiplegia. 

A curious and noteworthy phenomenon in these early hemiplegias 
is the associated movements. When a movement is performed on the 
well side, a lesser but corresponding movement is automatically per- 
formed on the paralyzed side. 

Much more common in childhood hemiplegia are the symptoms of 
cerebral irritation. They consist chiefly of choreiform, athetoid and 
trembling movements. Involuntary, irregular, incoordinated jactita- 
tions occur in the limb and resemble exactly a true chorea except in 
being so localized. They have been more or less present in every case 
that I have examined. The frequency and distribution of these post- 
hemiplegic choreas throw considerable light upon the probable patho- 
genesis of all forms of chorea. The athetoid movements often observed 
in these cases consist of slow, deliberate, wormy, wax-like flexion and 






THE NON-NEURONIC DISEASES 86l 

-extension, especially of the lingers and hand. They give to the move- 
ments and attitude an appearance of excessive affectation. Athetosis 
may occur in the leg as well as in the arm. One limb may even be 
choreic and another athetoid. In some exceptional cases an intentional 
tremor, such as is observed in disseminated sclerosis, may be detected. 

The cranial nerves may be implicated, causing strabismus, speech 
disturbances, difficult deglutition and other signs of bulbar disease. 
The motor character of all these manifestations is so overwhelming that 
one is prone to regard the lesion as solely one of the motor area of the 
cortex. It would upset, or at least greatly confuse, the accepted patho- 
genesis of these cases if no sensory symptoms were ever to have been 
found. As it is now believed that the sensory elements of the cortex 
are largely intermingled with the motor elements, one would think that 
sensory symptoms ought to be more frequently met with. Two ex- 
planations are possible to account for their absence in the report of 
eases. In the first place, it is extremely difficult to examine sensation 
satisfactorily in children so young as these are and to get reliable re- 
sponses ; and in the second place, the lesion in a large, number of cases, 
perhaps the largest number, involves more particularly the motor 
part of the internal capsule, and only temporarily and indirectly affects 
the sensory part. Nevertheless in a few carefully examined cases 
hypaesthesia, Wernicke's mental tactile anaesthesia, hemianopsia and 
aphasia have been noted. 

In all of the cases of infantile hemiplegia, whether unilateral or 
bilateral, prenatal or postnatal, cerebral symptoms of an irritative and 
developmental character sooner or later announce themselves. Some 
of these have already been referred to, as, for instance, the cranial 
nerve disturbances, the aphasia, the hemianopsia, and the choreic and 
athetoid exhibitions. Most important, however, are the epileptic at- 
tacks and the mental deterioration. Epilepsy and imbecility are so fre- 
quent that when found in conjunction with the paralysis become almost 
pathognomonic. 

Nearly two-thirds of the cases are subject to epileptic at dicks. 
Spratling finds that the most potent, immediate and single cause of 
epilepsy is the cerebral palsies of early life. The attacks may come on 
soon after the convulsive stage or years after. Usually the paralysis 
has existed a year or two before the fits began. I have seen a case in 
which the convulsion was entirely epileptiform and in which the tit- 
soon ceased in spite of the high degree of hemiplegia. The tit may be 
of the Jacksonian or partial type, but more commonly it is generalized 
as in ordinary genuine epilepsy. Unilateral epileptiform convulsions 
and spasms, without loss of consciousness, are not uncommon. The 
fit is rarely as protean as it is in ordinary epilepsy, though one may 
not be surprised to see the severest kind of fits with the cry, the tongue 
biting, the Unconsciousness and the convulsions of the idiopathic dis 
ease. Even status epilepticus, followed by early death, ma\ occur. I 
lately saw a case in which the hemiplegia had left only the merest i 
in the hand, but the epilepsy was formidable. 

So severe a lesion as usually causes these infantile palsies could 
hardlv be expected to leave the mental faculties intact The mental 



862 THE NON-NEURONIC DISEASES 

zveakness, imbecility and even idiocy are usually the direct result of the 
damage done to the growing brain. On the other hand, care must be 
taken to discover, if possible, if the mental deterioration may not be a 
secondary result of the epilepsy, of loss of hearing, or absence of lan- 
guage from mere aphasia. In many cases the general intelligence is 
not much affected, but upon close examination it will be noted that 
there is some degree of irritability of temper, exalted emotionalism 
and other symptoms that are hy steroid in character. It is important 
always to note the degree of mental impairment, for the prognosis and 
possible improvement of the paralytic symptoms depend in large meas- 
ure upon the degree of mentality in the case. Moreover in those cases 
in which the psychic disturbances are the least the paralyses that have 
remained somewhat stationary occasionally undergo a slight change for 
the better after puberty. 

Cranial malformations, facial asymmetry, prognathism, defective 
teeth and other stigmata of degeneration are found in a certain per- 
centage of these early hemiplegics. The skull may be microcephalic or 
macrocephalic, flattened on the side, of the lesion or otherwise altered 
with depressions, fissures, etc. It is w r ell to carefully distinguish always 
true stigmata of degeneracy from the mere changes wrought in the 
bones and other tissues by such influences as pressure, disturbed local 
nutrition and delayed development. 

Diagnosis. — The diagnosis of a case of cerebral palsy of child- 
hood is not particularly difficult if the history of the case is we'll 
studied and the hemiplegic character of the paralysis, with the possible 
existence of cerebral symptoms, are taken well into consideration. As 
distinguished from a spinal palsy, these cases involve larger groups of 
muscles, have exaggerated reflexes, show no true muscular atrophy or 
electrical reaction of degeneration and are accompanied by cranial 
symptoms, epilepsy and mental disorders. 

The real differential diagnosis in these cases involves more par- 
ticularly the distinction between the unilateral hemiplegias, the diple- 
gias and the spastic paralysis of Little's type. It must be remembered 
■that they are all cerebral in origin and therefore are all hemiplegic. In 
regard to the character of the paralysis, it is the same in all of them ; 
being merely unilateral in some cases, bilateral in others. This indi- 
cates involvement of one or both hemispheres with such lesions as 
hemorrhage, embolism, thrombosis, meningo-encephalitis, encephalitis 
or simple agenesis. The pathological diagnosis is not always easy, 
because the same pathogenetic factors may underlie very different 
sets of symptoms. In general, however, it may be said that prenatal 
cases produce largely the Little's type of the disease in which a diple- 
gia of the lower limbs, with but little involvement of the arms and 
scarcely any of the mental faculties, constitutes the salient feature in 
the clinical picture, all depending upon simple cerebral agenesis, hem- 
orrhage, chiefly meningeal, or meningo-encephalitis. The natal cases 
or true birth palsies are in most instances due to meningeal hemorrhage. 
They are diplegic and involve the arms and the mental faculties rather 
more frequently than the preceding group of cases. In the postnatal 
cases and those following the infectious fevers hemorrhage, chiefly 



THE NON-NEURONIC DISEASES S63 

intracerebral, embolism and thrombosis are the more common causes 
of the paralysis. These cases are usually unilateral. They exhibit the 
pre-hemiplegic and post-hemiplegic choreic phenomena, and athetosis 
rather more frequently than the cases that are more distinctly diplegic. 
While epilepsy and mental deterioration are present in these cases, the 
imbecility and idiocy are rare as compared with the diplegic cases. As 
the paralysis in all of these cases may occasionally be slight and the 
epilepsy, chorea or psychic disturbance be very prominent, confusion is 
likely to arise in the differential diagnosis between these accompani- 
ments of congenital spastic palsy and ordinary epilepsy, chorea and 
insanity. A careful regard for the anamnesis, the character and 
distribution of the special symptoms and the results of treatment will 
make clear the real nature of the case in hand. 

Prognosis. — The cerebral palsies of childhood are chronic and 
incurable. Nervous elements that have been profoundly damaged or 
prevented from growing cannot be restored by human agencies. The 
course of the disease, the time and cause of death and other factors 
in its prognosis are determined largely by the appearance and course 
of particular symptoms. Hemorrhagic and acute encephalitic cases 
usually recede somewhat and some improvement in the resulting 
paralysis may be hoped for up to the end of the first year. After that 
it remains stationary, except in a few of the diplegic cases in which 
the mind continues intact, in whom some improvement may be looked 
for after puberty. Diplegic cases as a rule are more stationary than 
the simple hemiplegic. If, however, epilepsy and imbecility develop, 
the prognosis becomes bad and the asylum is usually their final refuge. 
The absence of mental disorder secures a better prognosis for the 
paralysis. The diplegia of Little's type therefore can often be mark- 
edly improved, as cerebral disturbances other than the double hemi- 
plegia are relatively infrequent. 

Chorea, athetosis and contractures are unfavorable symptoms. 
They usually remain in spite of all kinds of treatment. Epilepsy may 
come on late or early. It may pass at any time into status epilepticus 
and destroy the patient. The presence of true stigmata of degeneracy 
renders the prognosis unfavorable. Aphasia usually disappears, though 
dysarthria may continue permanently. Some hemiplegics reach an old 
age, others succumb about the time of the change of life or pass into 
actual insanity. 

Treatment. — The treatment of the onset must be in accordance 
with the pathological diagnosis. Hemorrhage, embolism, thrombosis, 
encephalitis have their own particular lines of treatment. In febrile 
cases ice bags, antipyretics, cathartics, etc., are all in order. The 
treatment should be carried out on general principles. Rarely, h<>w 
ever, is the practitioner called upon to treat the early onset of the 
trouble. As a rule lie is consulted only when the paralysis lias been 
some time in existence. 

Mechanical and pedagogic treatment 1^ about all that can be in 
stituted. There is no medicine with which to combat the changes in 
the central nervous system. 'Tonics are all that ran be thought of in 
the way of medicinal agents. Daily massage, electricity and pass 



864 THE NON-NEURONIC DISEASES 

movements may be employed for the paralysis. Epilepsy is to be 
treated as usual with the careful administration of the bromides. This 
symptom, like the chorea and athetosis, is not very amenable to me- 
dicinal management. Contractures should be overcome by stretching, 
forcible replacement, splints, tenotomy and other well-known orthor- 
psedic and surgical procedures. 

Education, discipline, gymnastics and systematized exercises can 
sometimes accomplish very gratifying results in cases in which the 
intelligence is preserved. I would warn against over-exercise in car- 
rying out this line of treatment. Exhaustion must be guarded against. 
With this single, proviso, it may be truthfully said that these patients 
cannot be encouraged too much to use and use systematically as well 
as they can their paralyzed limbs. 

Trephining and craniectomy as suggested by Lannelongue have 
been tried in some of these cases ; clots have been removed and cysts 
have been evacuated. The ultimate results have not been sufficiently 
favorable in a large enough number to pronounce definitely upon the 
utility of these surgical measures. Further experimentation is needed. 

ENCEPHALITIS. 

By the term encephalitis is meant an inflammation of any part 
of the encephalic mass, particularly the gray substance. The inflam- 
matory process may be acute or chronic, diffuse or focal, suppurative or 
non-suppurative, simple, toxic, exudative and hemorrhagic. It may be 
primary and limited to the gray substance, or it may be secondary and 
associated with a meningitis or other inflammatory process. There are 
many forms of encephalitis, therefore, some of which will now be dis- 
cussed, while others will be considered in other chapters. 

Chronic menin go- en cephalitis, or dementia paralytica, is of suffi- 
cient dignity to have a chapter by itself. The encephalitis sometimes 
found in connection with chorea insaniens, acute mania, delirium 
tremens, the maniacal form of exophthalmic goitre and hydrophobia, 
will be noticed when these diseases are discussed. The spastic paralysis 
of childhood is in some instances doubtless due to a foetal meningo- 
encephalitis, while the hemiplegia of children has been thought by 
Striimpell, though not by others, to be the result of a polio-encephalitis, 
a sort of homologue of poliomyelitis. Indeed, after infectious diseases 
there sometimes is found a diffuse encephalitis, which constitutes a 
part of a disseminated my elo- encephalitis. Disseminated encephalitis 
is the name sometimes given to the cerebral form of multiple sclerosis. 
Syphilitic encephalitis will be noticed under the head of syphilis of the 
nervous system. When treating of the ocular palsies and of diseases of 
the medulla oblongata respectively, mention will be made of superior 
and inferior hemorrhagic polio-encephalitis. 

It will be observed that these forms of encephalitis are either parts 
of a larger inflammatory process, or are so focalized as to be dis- 
cussed to a better advantage elsewhere. 

In this section two of the principal forms of the disease only will 
be treated of in detail — namely, the acute non-purulent hemorrhagic 



THE XOX-XEURONIC DISEASES 865 

encephalitis and the acute and chronic purulent encephalitis, or cerebral 
abscess. 

ACUTE HEMORRHAGIC ENCEPHALITIS. 

This is a scattered, focal, non-suppurative inflammation of the 
brain, characterized especially by spots of intense congestion with 
capillary hemorrhages. 

Etiology. — Though many causes have been credited with this 
disease, it is now pretty well established that some form of infection 
is the cause in the vast majority of cases. Influenza seems particu- 
larly blameworthy, many cases always occurring during an epidemic. 
It has followed measles, scarlet fever, pneumonia, erysipelas, pertussis, 
mumps and diphtheria. It has been seen in the victims of an ulcerative 
endocarditis. According to Osier, the most typical encephalitis ac- 
companies the meningitis of cerebro-spinal fever. Dana adds typhoid 
and typhus to the causative infections and says that it may occur in 
connection with the puerperal state. It is an open question whether 
it can result from acute alcoholism without coincident infection. Sun- 
stroke, Dana believes, has produced it, while some observations would 
seem to indicate that it may follow simple traumata. It is not im- 
probable that the traumatic encephalitis may be different from the 
infectious, so little is known about it. It is a common observation, 
however, that a simple contusion or local shock often serves to estab- 
lish a nidus for the bacteria or other microorganisms of a latent infec- 
tion to begin their work in. 

Pathology axd Pathogenesis. — The disease process is seen post 
mortem as an acute inflammation of the exudative and hemorrhagic 
type. The capillaries are engorged; the tissues are hyperaemic, swol- 
len and moist; the vascular sheaths are distended with fluid: there is 
an infiltration of leucocytes ; and in the older cases there are granu- 
lated cells and proliferated gliomatous cells. There is irritation and 
degeneration of the nervous elements. All of which arc seen to be 
limited to more or less circumscribed areas scattered about in the cere- 
bral cortex, central ganglia, centrum semiovale and cerebellum. Some- 
times these extend into the medulla and pons, giving rise to the 
form of the disease known as acute bulbar myelitis and acute inferior 
polioencephalitis. The process may even reach as far down as the 
cord, thus involving the whole cerebro-spinal axis and giving rise to 
the disease known as disseminated myelo-encephalitis. According i«- 
Oppenheim, a combination of encephalitis with acute anterior polio 
myelitis has been observed, and it was Strumpeirs idea that tin- acute 
encephalitis, which he believed to be the cause of infantile cerebral 
paralysis, was in some way related by analogy with inflammation <»t' tin- 
anterior cornua in infantile spinal paralysis. Many observers have 
noted a sinus thrombosis with this encephalitis, while in severe > 
Oppenheim has found a marked ventricular exudate, meningeal hyper 
semia, etc. When the procr mild one with recovery, minute 

sclerotic foci may be left in the brain. In the severer cases an extensive 
softening may occur and larger hemorrhages, even terminating in a 
massive apoplexy, as once seen by Dana. 



866 THE NON-NEURONIC DISEASES 

Symptoms. — This disease is most frequently observed in girls and 
children of tender years. They rarely complain of any premonitions, 
for the headache, the malaise, the mental apathy may be the result of 
the infection rather than of the encephalitis. The latter usually an- 
nounces itself abruptly by a chill, a sadden rise of temperature and a 
stuporous, semiconscious condition that closely simulates an apoplectic 
attack. Unlike apoplexy, however, the pupils react to light, the re- 
flexes remain unaffected and the coma is not so deep. The pulse be- 
comes quick and feeble and the respirations are rapid. Unlike menin- 
gitis, there is no stiffness of the back of the neck and no signs of a 
generalized cortical irritation. In many cases the coma rapidly deep- 
ens and in twenty-four or forty-eight hours the patient is dead. 

Sometimes the disease runs a milder and more protracted course 
of several weeks, with remissions and exacerbations. In such cases 
there may be a temporary clearing up of the mental stupor, but there 
will be left a monoplegia or a hemiplegia. Aphasia is not unlikely to 
occur and even cortical epilepsy and hemianopsia. In some cases 
optic neuritis was seen. The location and nature of the lesions are 
various and hence there is no strict uniformity in the clinical picture. 

Diagnosis. — Meningitis is the disease with which hemorrhagic 
encephalitis is most frequently confounded. Sometimes it is absolutely 
impossible to make a differential diagnosis. In encephalitis, however, 
the absence of the irritative signs, like the muscular rigidity of the 
back of the neck, the normal pupillary reaction, the absence of Kernig's 
sign, the absence of cutaneous hyperesthesia, involuntary cry with the 
presence of paralytic manifestations, epileptiform attacks and a history 
of infection, will give much assistance. The differentiation of a tuber- 
culous meningitis might be made by lumbar puncture and the discovery 
of a tuberculous process in the lungs or bowels. 

Prognosis. — The prognosis is grave, but not necessarily bad. Re- 
covery occasionally occurs with a convalescence lasting for weeks, 
months and sometimes years. Rarely does recovery take place devoid 
of all permanent defect. A hemiplegia, multiple sclerosis or mental 
deterioration may be the after-clap. 

Treatment. — Rest, both mental and physical, absolute rest, is the 
best that can be done in the way of treatment. In the beginning active 
purgation with calomel, croton oil and stimulation of the kidneys are 
indicated. Cold compresses and an ice-bag to the head, venesection, 
leeches all constitute good routine measures. The feet may be kept in 
hot water. Stupor with a high fever would indicate the need of 
aconite. Strychnia might be used in asthenic cases. In all classes of 
cases the nourishment should be kept well up and the excessive pain 
should be controlled with morphine. Chloral and the bromides may 
be used to combat sleeplessness and irritability. Oppenheim says that 
in one case that recovered calomel in large doses — even to the point of 
producing stomatitis — was used. There is nothing to be said particu- 
larly of the after-treatment and the management of the convalescence. 
It is about the same as it would be in a case of ordinary cerebral hem- 
orrhage. 



THE NON-NEURONIC DISEASES $6/ 

ACUTE SUPPURATIVE ENCEPHALITIS. 

(CEREBRAL ABSCESS.) 

Idiopathic brain abscess is practically unknown, though at rare 
intervals a case is observed in which no cause can be found for the 
suppurative process. It is probable that in such cases a direct cause 
was present sometime, but so long ago or so unobtrusive was it that it 
had been quite forgotten. Cerebral abscess is then the result of an 
acute suppurative encephalitis, focal or diffuse, produced by microor- 
ganisms introduced into the brain from without. 

Etiology. — Acute suppurative encephalitis is always the result of 
bacteria that have gained entrance into the brain substance in three 
general ways. It is etiologically due, therefore, to direct injury of the 
head, to extension of a suppurative process in the tissues immediately 
surrounding the brain, or to a metastatic transference of the bacteria 
by the blood from some 1 emote center of suppuration in the body. 

It is estimated that about 30 per cent, of the brain abscesses are 
due to traumatism. A fracture or puncture of the skull is the usual 
form of the injury. In some cases a foreign body has passed into the 
brain; in others a mere contusion of the scalp has been sufficient to 
give entrance to the germs. The majority of the traumatic cases have 
been complicated fractures in the frontal and parietal parts of the 
head. Operations within the nasal and orbital cavities have been re- 
sponsible in a few instances. Bone fracture is not absolutely necessary 
for the admission of the germs, since infected emboli and implication 
of the lymphatics are fully adequate. It is clear how some of these 
slighter traumatic causes may readily be overlooked when it is remem- 
bered that sometimes the cerebral symptoms do not announce them- 
selves until many years, ten, twenty and thirty even, after the injury. 

Somewhat more than a third of the cases are due to extension of 
the suppurative process or the transmission of the microorganisms from 
chronic otitis media and disease of the mastoid cells. Of these ear cases, 
it is found that about 85 per cent, are due to chronic suppuration, and 
the remaining 15 per cent, to acute suppuration in the ear. The number 
of cases due to mastoid disease is less than those due to otitis media. 
Most of these ear troubles follow the infections fevers of childhood. 
They sometimes continue many years, undergo remissions, or even 
disappear entirely long before the evidences of brain trouble declare 
themselves. In a considerable number of cases I have been struck with 
the statement of the patient that many years before she had had a 
running from her cars for a time, but her physician had succeeded in 
stopping the discharge. Sometimes there is perforation of the tympanic 
membrane in these eases and even earies of the petrous bone, with 

periodical attacks of otorrhcea. In rare instances the suppurative 
process has extended from the nasal or orbital cavity; or there has 
been caries of the neighboring bones, such as the ethmoid, sphenoid, 
superior maxilla. 

The distant sources of infection are numerous and varied. [n 



868 THE NON-NEURONIC DISEASES 

some way by metastasis the germs are carried to the brain from the 
most remote parts of the body. Even a purulent osteitis or arthritis 
may in rare instances be the origin of the brain abscess. It is stated 
that about one-fifth of the cases are due to pyemic emboli from the 
thoracic cavity. Bronchiectasis, empyema, pulmonary gangrene or 
abscess, purulent pericarditis, ulcerative endocarditis, have been fol- 
lowed by brain abscess. The latter has been attributed to abscesses in 
the abdominal viscera, to actinomycosis and to simple thrush. Tubercle 
bacilli and pneumococci have been recovered from it. In these cases 
the abscesses are apt to be small and multiple. 

Cerebral abscess occurs more frequently in males than in females, 
and oftenest between the ages of ten and thirty. 

Pathology and Pathogenesis. — Abscesses may occur in all parts 
of the brain and are usually associated with signs of traumatism, ear 
trouble or remote suppurative foci. They may be outside of the dura 
{extradural), inside of the dura (subdural) , in the cortex or in the cen- 
trum semiovale. Multiple abscesses, as many as a hundred having been 
counted in one case, may be no larger than a pea; simple abscesses 
may attain the size of an orange, or even occupy one whole hemi- 
sphere. Cerebral abscesses are usually single ; cerebellar are more apt 
to be multiple. As a rule the abscess lies just beneath the seat of 
injury; occasionally, however, it is found on the opposite side, the 
result of the contre-coup. Traumatic abscesses are largely extradural 
and are accompanied by meningitis. They are more frequent in the 
frontal and parietal lobes, as the front of the head is most exposed to 
blows. Otitic cerebral abscesses are found usually in and just beneath 
the gray cortex of the temporo-sphenoidal lobe on the same side as 
the affected ear. Abscesses due to mastoid disease are generally located 
in the cerebellum. In the pons and medulla they are rarly seen. 
Chronic abscesses are round in shape and encapsulated within a fibrous 
wall, which takes about four weeks to form. 

There is nothing unique about the formation process of these 
abscesses. The usual pyogenic microorganisms are found within them, 
especially the streptococcus pyogenes, the staphylococcus pyogenes 
aureus, albus and citreus. They undergo the usual transformation of 
red and yellow softening, with crowding of the leucocytes, infiltration 
of inflammatory exudate, destruction of nerve cells and processes, ap- 
pearance of granular corpuscles, etc. 

Symptoms. — The symptoms of brain abscess arrange themselves 
into three groups — namely, those of a general character due to the 
presence of a septic process, those due to intracranial pressure from 
the presence of the abscess, and those that depend upon the particular 
location of the abscess within or upon the encephalic mass. 

In the history of every cerebral abscess, especially if it is clonic. 
practically all of these three groups of symptoms have been more 
or less in evidence sometime or other. They may not all be present 
simultaneously, and the last or localization group is the one most fre- 
quently absent. Moreover, they do not all exist with the same degree 
of prominence. In one case the septic symptoms may be the most 
prominent, as is often the case in the pyaemic metastatic multiple 



THE NON-NEURONIC DISEASES 869 

abscesses ; in another case the pressure symptoms may be the only 
markedly noticeable ones ; in a third case there may be distinct local- 
ization symptoms, but the septic and pressure signs may be so slight 
or evanescent that one hesitates to diagnose the neoplasm as an abscess. 
It is calculated that in about 8 or 10 per cent, of cases the symptoms 
are so slight that they are overlooked entirely and the abscess is not 
discovered until after death. 

With all this variability and uncertainty about its symptomatology, 
a brain abscess can pretty nearly always be strongly suspected, if not 
absolutely diagnosed, if the history and physical examination are gone 
into minutely and conscientiously. This applies with special force to 
the early diagnosis of the trouble and is of paramount importance 
because the earlier the diagnosis is made the brighter is the hope from 
surgical intervention. 

Strictly speaking, there are no prodromes, but what are sometimes 
called prodromes are early symptoms in one case or even late symptoms 
in a mild or latent abscess. A slight headache, a feeling of malaise, oc- 
casional chilliness, attacks of cardiac palpitation, sudden and unac- 
countable slight elevations of temperature, certain fugitive vasomotor 
manifestations, occasional attacks of insomnia, an annoying degree of 
slight mental hebetude with a feeling of depression and anxiety — in a 
word, all the signs of a mild form of toxcenne neurasthenia — may con- 
tinue for months and years before more definite indications declare 
themselves. I saw a case that misled, by reason of the indefiniteness 
its clinical manifestations, many diagnosticians for seventeen years, 
during which period the patient had been a number of times suspected 
of being insane, being sent each time to an asylum and discharged as 
cured after several weeks. When T saw her the clinical picture was 
clear enough to warrant a positive diagnosis of abscess, from which 
the patient finally died in coma several days later. 

It is difficult to say usually how much of these early symptoms are 
due to the sepsis, especially if there are other septic foci elsewhere in 
the body, and how much to the cerebral neoplasm alone and its non- 
septic disturbances. The headache, for instance, in these circumstances 
cannot always be assigned to the toxic disturbance or the pressure. 
Such a group of manifestations, neurasthenic and phrenasthenic in 
character, if associated with a history of hearl injury, abscess t'<>ci else- 
where and especially ear trouble, should always put the physician on 
his guard and awaken a lively suspicion of a possible cerebral abscess. 

It is in the acute abscesses, following wounds about the head, and 
in the exacerbations of the chronic abscesses from the other c.c 
that the constitutional septic symptoms make themselves particularly 
obvious. They are the same as symptoms that occur in all septic 
poisoning — namely, chills, variable temperature, anorexia, coated 
tongue, constipation, headache, dullness of mind, general feeling 
malaise and emaciation. A general cachectic condition with icteric 
discoloration of the skin, loss of appetite, irritability, ness and 

mental confusion sometimes obtain. Tin- fever is vn\ irregular and 
slight. In some cases it is entirely absent. In no case does it i 
last verv long. Subnormal temperature is », , frequent as t<» be a 



&7° THE NON-NEURONIC DISEASES 

highly suggestive symptom. The pulse may be rapid and unsteady; 
often it is very slow, beating only 40 or 30 to the minute. With dis- 
turbance of the pulse and sudden elevation of the temperature the 
headache increases in severity. The respiration is sometimes irregular 
and slow. 

The pressure symptoms of brain abscess are much the same as 
those of any form of intracranial growth. They are headache, mus- 
cular twitching and rigidity, local and generalized convulsions, epilepti- 
form phenomena, paralysis, vertigo, vomiting and mental stupor. Con- 
traction and dilatation of the pupils, disturbed vision, optic neuritis, 
tinnitus aurium and other symptoms dependent upon the cranial nerves 
sometimes occur. The subnormal temperature, retarded pulse-beat 
and respiration and certain vasomotor disturbances are in part due to 
the intracranial pressure. 

Of all these pressure symptoms the headache is probably the most 
reliable. It is generally constant and severe and definitely localized 
by the patient. He usually points to a particular spot on the head, 
not unfrequently behind the ear or in the occipital region, percussion 
upon which causes him to wince. Sudden jars and disturbances of 
the heart action, as well as the onset of a febrile exacerbation, cause 
the headache to become almost intolerable. The same result follows a 
sudden flash of light or a sudden noise. Though more or less constant, 
the pain is often worse at night, causing insomnia. Partly on account 
of this constant pain and partly on account of the pressure and general 
septic condition, the patient becomes extremely melancholy, depressed, 
apathetic and stupid. Occasionally marked delirium occurs and passes 
into coma, which in turn terminates in death. Sometimes the headache 
diminishes and I have known it to vanish entirely after a time without 
any disappearance, however, of the other suspicious signs of abscess. 
Not always do these headaches indicate the location of the abscess. 
It may occur that the headache is frontal, while the localization symp- 
toms point to an occipital abscess. A characteristic of them having 
some diagnostic value is that they are usually unrelieved by medica- 
tion. 

Vertigo and vomiting are frequent symptoms, the latter especially 
so in cerebellar abscess. 

Round about the abscess minute hemorrhages occur. These being 
more marked in the early stage of the process, they, with the abscess 
itself, give rise to irritative symptoms, followed sooner or later by 
paralysis. Hence in cortical abscesses there are epileptic phenomena. 
focal and generalized, with monoplegic symptoms. In this irritative 
stage it is hard to determine at times whether the symptoms are due 
solely to the abscess or to a meningitis. Not unfrequently such 
abscesses are accompanied by a local meningitis, and then the symp- 
toms will be of a combined character. It is in the traumatic abscesses 
that the meningitis mostly occurs and the irritative symptoms are the 
more prominent. 

Among the pressure symptoms the optic neuritis, when present, is 
a most valuable one. It is of the so-called choked disc variety, Knies* 
obstructive optic neuritis. It is never so marked nor is it so con- 



THE NON-NEURONIC DISEASES 87 1 

stant as it is in cerebral tumor. It is believed that ocular symptoms, 
including the motor and pupillary, are to be found in about half of 
the cases. Witherspoon asserts that cerebellar abscess gives rise to 
optic neuritis in from 75 to 80 per cent, of cases, whereas cerebral 
abscess is responsible for it in only about 30 or 40 per cent. 

The focal symptoms are of much consequence, though unfortu- 
nately they are often too indefinite. Abscesses lying in the so-called 
latent parts of the brain cannot, of course, be localized by any focal 
signs. Traumatic abscesses of the frontal lobes are usually devoid of 
localizing symptoms unless they are large or situated in the posterior 
part of the lobe, especially on the left side. By encroaching upon the 
precentral convolution, the base or near the posterior part of the third 
frontal, they may cause, along with psychic confusion and other mental 
disturbances, Jacksonian symptoms, aphasia, parosmia and ataxia. 
Hemiplegia or monoplegia may occur with abscesses located in and 
about the cortical Rolandic region. The metastatic embolic abscesses 
from septic foci in the thorax are apt to form in the area sup- 
plied by the Sylvian artery and give corresponding focal 
signs. The otitic abscesses are usually single and form in the tem- 
poro-sphenoidal lobe. The hearing consequently is affected. There 
is mind-deafness, auditory aphasia, and possibly by pressure amnestic 
aphasia and oculomotor paralysis, the frequency of which in this form 
of abscess has been pointed out by Wernicke. These abscesses when 
deep affect the underlying motor, sensory and optic conducting tracts. 
Hence there may be opposite-sided hemiparesis with rigidity or con- 
tracture. Or there may be hemiansesthesia and hemianopsia. In a case 
observed by Jansen and Oppenheim there were from a right-sided 
temporal lobe abscess left hemiparesis, hemihypaesthesia, hemianopsia 
bilateralis sinistra and conjugate deviation of the head and eyes to- 
ward the right. Ptosis from paralysis of the third nerve and internal 
strabismus from the sixth are rather common in temporal lobe 
abscesses. 

Blindness may occur when the abscess is in the occipital lobes, 
while hemianopsia occasionally accompanies abscesses of the occipital 
lobe and of the lower part of the parietal lobe. 

Cerebellar abscesses are usually due to mastoid disease and de- 
clare their presence by such localizing symptoms as ataxia, suboccipital 
headache, vomiting, cervical rigidity and rarely by bilateral amaurosis 
and pressure on the adjoining cranial nerves and their nuclei. Ac- 
cording to Macewen, the knee-jerks were absent in some eases ^\ 
cerebellar abscess. 

Abscess of the pons and medulla oblongata is very rare, yet when 
present has the typical bulbar symptoms to complete its clinical picture. 

Occasionally an abscess bursts into the ventricles, giving all the 
symptoms of a profound apoplectic stroke; namely, convulsions, fol- 
lowed by paralysis, deep coma, etc., all quickly terminating in death. 

Diagnosis. — In spite of the fact that cerebral abscesses an 
often latent and therefore cannot be diagnosed at all. and even when 
they have symptoms these are so often indefinite and variable, the gen 
era'l clinical picture is sufficiently unique and characteristic to enable 



872 THE NON-NEURONIC DISEASES 

one in a large majority of cases to form a diagnosis, or at least a 
strong suspicion, especially when there has been a history of trauma- 
tism, local infection in the ear or septic processes elsewhere about the 
body. It is upon the history of the case, with the present symptomatol- 
ogy viewed en masse, rather than in detail, that the strongest diagnosis 
of cerebral abscess is made. It is the tout ensemble of the picture that 
here indicates the nature of the trouble, and not this or that particular 
symptom or small group of symptoms. 

There are quite a number of diseases with which brain abscess 
might be readily confused. This is because of the multiplicity of its 
symptoms, all depending upon so many different factors. From 
meningitis, particularly external purulent pachymeningitis or extra- 
dural abscess, it is distinguished by the greater degree of intracranial 
pressure, the more definite localization of symptoms and the absence 
of the characteristic irritative signs like the cervical rigidity, pupillary 
contraction and Kernig's symptom. In diffuse purulent meningitis, 
differentiation is often extremely difficult. The irregular and low 
fever, the slow pulse, the localization signs and the absence of most 
of the irritative symptoms of meningitis, such as the hyperesthesia, the 
muscular rigidity, the twitchings, the spinal symptoms and the mental 
restlessness are enough to make in typical cases a differential diagnosis 
easy. Lumbar puncture will assist in some cases. 

Other forms of meningitis that must be eliminated in the diagnosis 
are a localized meningo-ence phalitis and serous meningitis and tubercu- 
lar meningitis. In typical cases the differentiation is not difficult when 
one recalls that abscess produces only temporary or transient irritative 
symptoms, that its febrile characteristics are quite unlike those of 
meningitis, and that it has, like tumor, certain more or less definite 
intracranial localization symptoms. In the combined cases it is diffi- 
cult, but if the case is a combined one we can neglect the meningitis 
and diagnose the abscess, or in other words, a differential diagnosis is 
not imperatively called for. The distinction between brain abscess 
and the traumatic neuroses, especially when the former is due to a 
traumatism, must be carefully made. A careful consideration of the 
symptomatology of the traumatic neuroses, hysteria and neurasthenia, 
and its unlikeness to that of abscess, with its distinct organic and septic 
symptoms, ought, it seems to me, to make a differentiation here a 
matter of no very £reat difficulty. 

Tumor of the brain has many symptoms in common with those 
of abscess. In tumor, how r ever, the headache and optic neuritis are 
more constant and pronounced, the development of the disease is slow- 
er, there is absence of fever and septic symptoms and altogether more 
of a uniformity, steadiness and chronicity about the clinical picture. 

Prognosis. — Brain abscesses are both acute and chronic. Both 
forms are sooner or later fatal if not interfered with surgically. It 
is a rare thing indeed for an intracranial collection of pus to break 
into the nasal, orbital or buccal cavity ; still more rarely does it open 
out directly on the head. A spontaneous cure by this or any other 
means is not to be looked for. These cases are as fatal ultimately 
as any. 



THE NON-NEURONIC DISEASES 873 

Cerebral abscess often runs a long course, with occasional remis- 
sions and changes in its symptomatology. When single and encap- 
sulated it may remain in a semi-quiescent state many years. Then it 
suddenly bursts into the neighboring ventricle or through the mem- 
branes and brings on alarming symptoms, with delirium, coma and 
death in a few hours. I have seen death follow a semicomatose condi- 
tion lasting several days. This coma is a certain indication of an early 
demise. 

Without interference, therefore, the prognosis of cerebral abscess 
is bad. With surgical intervention a little more than half the traumatic 
cases, and a little less than half the otitic cases, are saved and cured. 
Of course, the resulting scar tissue and damaged cerebral cells will 
in all probability leave some focal symptoms of a permanent character. 
Occasionally an abscess unfortunately recurs after a successful opera- 
tion. The most favorable location for an operable abscess is the tem- 
poral lobe ; the cerebellum is somewhat less favorable. 

Treatment. — The treatment cf brain abscess resolves itself into 
prophylaxis and surgkal evacuation. In the antiseptic management of 
fresh wounds about the head much can be done to ward oft intracranial 
infection. This is an added argument in favor of the maintenance of 
rigid asepsis in all operations in the nose and mouth, about the eye and 
ear. Forcible injections and irrigations, especially in the ear, must not 
be resorted to. Pus when present must be drained oil, and under no 
circumstance must a running from the ear be checked by closure of 
the opening. I repeat that the mere cessation of an otorrhoea has 
seemed to me in a number of cases to have been too fondly assumed as a 
cure of the ear disease. 

When an abscess of the brain is finally diagnosed, and its location 
is favorable for operation, there should be no further temporizing, but 
immediate evacuation with v drainage should be insisted on. There 
is no other treatment for an abscess. I cannot see the wisdom cf 
Oppenheim's suggestion to first try if removal of the pus in the tar or 
in the extradural region will relieve the cerebral symptoms in a 
where the diagnosis of uncomplicated otitic cerebral abscess can be 
definitely made. As a preliminary measure these operations will be 
done anyhow, and if the cerebral symptoms are thereby relieved in part, 
it is no proof that a cerebral absce-- does not exist. Therefore instead 
of recommending a measure that might readily be interpreted into 
meaning a delay, it seems to me the better part of wisdom to advise that 
every case of otitic cerebral abscess, where a diagnosis can be definitely 
made and where the location of the abscess is favorable for operation, 
should be operated at once or as early as possible. In view of their 
almost certain fatality without operative measures, I do n<>t feel that 
external purulent pachymeningitis, circumscribed purulent meningitis, 
diffuse purulent meningitis, sinus thrombosis or even beginning pyaemia 
should be looked upon as contra-indications t-> operative interference. 
The patient's life is never safe so long a- there is a nidus of pus within 
his cranium; it is safe in a large proportion i when that nidus 

of pus is opened and drained. 

Some operators report recovery by surgical \\^ in the 



874 TH E NON-NEURONIC DISEASES 

cases of metastatic multiple abscess. Such cases, however, must nec- 
essarily be very rare. Moreover, so often is the original source of in- 
fection incurable that it would seem to be an almost useless task to 
attempt to cure, under such hopeless conditions, the trouble in the 
brain. 

ACUTE DELIRIUM. BELL'S MANIA. 

So varied are the opinions in regard to the nature of this brain 
disease that many names have been applied to it. The one that I have 
here selected is the one most commonly used. In the form described by 
Bell, and most of the authors who have followed him, there are no 
constant, distinctive post-mortem findings. Ford, Wood and others 
believe that it is a type of inflammation and should therefore be classi- 
fied as a menin go -encephalitis, or a periencephalitis. I am inclined to 
classify it with the brain inflammations in spite of the fact that the 
microscopical findings are negative. 

The symptoms are those of a profound intoxication, autochthonous 
or otherwise, and in a few cases which have been carefully examined 
signs of a diffuse inflammation have been discovered. The poison, 
either by reason of its extreme virulence or the peculiar susceptibility 
of the patient, so overwhelms the brain cells in some cases that death 
ensues before histological changes have had time to take place. In other 
cases by reason of the weaker character of the poison, the longer con- 
tinuance of its action or the greater power of resistance on the part 
of the patient, histological changes of a diffuse, inflammatory character 
are able to develop and so are revealed post mortem. Therefore, as in 
the analogous instance of Landry's paralysis, it seems to me that in 
Bell's delirium we are witnessing merely an early stage of a high de- 
gree of intoxication, which, if granted time to pass into a later stage, 
without the sudden intervention of death, would frankly declare itself 
as a form of toxic, diffuse encephalitis. This will be more clearly 
brought out in the further discussion of the disease. 

Etiology. — Most authors find that women are much more subject 
to the trouble than men, and that it occurs most frequently between 
the ages of twenty-five and forty-five. It occurred in a girl of eleven 
years of age in a case of Morel, quoted by Maudsley. Heredity does 
not seem to play a very prominent role. Emotional strain, distress, 
anxiety, worry, mental shock are more important as causative factors. 
Schule has attributed it to severe physical pain. Sunstroke, injury 
to the skull and the climacteric have been mentioned in its etiology ; 
to these must be added alcoholism, of course. More significant than 
any of these causes are those that involve infection. It has followed 
typhus and typhoid fever, epidemic, influenza, erysipelas and some skin 
affections. It has accompanied exhaustive dysentery, puerperal sepsis 
and epileptic attacks. Wood, Hurd, Berkeley, Dercum, Briand, Rohe 
and others consider a toxaemia or infection to be the primary cause, if 
not the essential cause in all cases. 

Pathology and Pathogenesis. — Some authors, as, for example, 
Pritchard, affirm pathology shows that under the name Bell's disease 
we have heretofore been describing two fundamentally different, though 



THE NON-NEURONIC DISEASES S75 

symptomatically similar, conditions of disease ; the one organic, with 
a variable but always demonstrable pathology, essentially inflammatory. 
due to toxines, infection or trauma, the lesion varying from a gross 
menin go-encephalitis to limited lepto-meningitis or arachnitis, the 
other non-organic, or at least with findings indicating simply nutritional 
or dynamic changes without adequate or other than conjectural ex- 
planation either as to their etiological nature or pathological signifi- 
cance and interpretation. Most authorities would assume that this 
second, non-organic class was due to an intoxication. If this be so, 
there is no difficulty in recognizing both classes of cases as but two 
iypes of the same disease, for they agree in everything except the 
pathological findings, and in respect to this discrepancy the case is the 
same, as we have seen in Landry's paralysis and certain inflammatory 
conditions of the cord. The so-called non-organic cases are but the 
earlier stages of an overwhelming intoxication, which, given more time, 
less virulence or other conditions, would go on to provoke distinct 
gross signs of a diffuse inflammation. Granting the frequent con- 
founding of other forms of inflammation, such as traumatic meningitis 
-and encephalitis, with this disease, the findings are yet sufficiently sug- 
gestive of an incipient inflammation in the later stages of Bell's 
delirium. There is congestion of the vessels of the meninges and of 
the cortex and engorgement of the veins. In two cases examined by 
Osier there were perivascular exudation and leucocytes in the lymph 
sheaths and periganglia spaces. In Pritchard's case the pia mater 
was markedly cedematous and the blood vessels injected. The capil- 
laries of the cortex showed marked distention, but no petechial hem- 
orrhages were observed. The choroid plexus of the ventricles was 
cedematous. The cells were practically unchanged. ( )sler urges that 
a careful examination in fatal cases be always made of the lungs and 
ilium. In the majority of cases he says there is engorgement of the 
bases of the lungs and even deglutition pneumonia. I found this in a 
recent case of my own. Tnough the nature of the disease is thus not 
positively demonstrated, the findings point strongly to a condition of 
acute, severe infection. 

SYMPTOMATOLOGY. — The symptoms of this disease are almost en- 
tirely mental, which doubtless accounts for some of its names, as well 
as for the fact that it has been so long regarded as a pure psychosis. 
There are, in almost every case when closely studied, seen t<> he symp- 
toms that point to organic lesions and disturbances in the brain cortex. 
The abruptness of onset, the rapid advancement, the extreme violence, 
the utter incoordination and unsystematized character of them, their 
frequent remission, and their ultimate subsidence in death or dementia 
are the striking traits about the mental manifestations. 

The patient will be resting quietly when all of a Midden there will 
be a terrific outburst of wild delirium and intense frenzy. This i^ hys 
tero-maniacal in general character and is associated with hallucina- 
tions, great violence and motility, destructiveness and incoherence. 
Chattering and talking is incessant. The speech is absolutely uncoil 
trolled SO that obscene, boastful. lasci\i«uis ideas air voluminou 
poured forth. Laughing and screaming, alternating with wild singing 



876 THE NON-NEURONIC DISEASES 

occur, all without the slightest trace of intelligence. The patient has 
been compared in this state to a maddened animal. The muscular 
movements are intense and constant until exhaustion puts an end to 
them. Vasomotor disturbances are obvious. Sleep is impossible.. 
Anesthesia and analgesia are apt to be complete. Food is obstinately 
refused. On account of all this the patient soon becomes utterly pros- 
trated and remains quiet with a more or less complete return to normal, 
consciousness. In a short time, however, another exacerbation comes 
on and the noisy, terrific scene is repeated. These remissions are a. 
striking feature of the disease. They are transient and become shorter 
and less frequent as the disease progresses. In them the patient may 
seem to have recovered complete health and for this reason they often 
give rise to false hopes. Pritchard says that delusions occur, especially 
in connection with the visual sense, and that strange and familiar per- 
sonalities arise. Shameless masturbation is practiced and attendants 
of the opposite sex are openly solicited. Sometimes in the speech there 
is observed a certain connected sequence and almost coherence, but the 
usual, absolutely unsystematized character of the ideas helps to dis- 
tinguish this trouble from a typical mania. Proper notions in regard 
to time, place and surrounding conditions are as a rule completely lost. 

Death almost always occurs in this disease and in the acute cases in 
about a week ; when partial recovery takes place the delirium is suc- 
ceeded by dementia, which remains more or less permanently. 

Such is the mental picture of these cases, but none of them are 
ever absolutely devoid of constitutional and somatic symptoms. The 
temperature usually rises rapidly, especially during the frenzy, and 
may attain to 105 degrees F. The pulse is variable, though it is always 
more or less disturbed. Both the temperature and the pulse as a rule 
remain above the normal. Convulsions and epileptiform manifesta- 
tions sometimes occur, as well as strabismus and various paralyses. 
Even more suggestive are the not unfrequent trophic manifestations,, 
such as alopecia, degenerative atrophy, petechias and other lesions of 
the skin and bones. Even bullae and pustules, with sores from abrasions 
and injuries, are frequently seen on the skin. The tongue is dry and 
apt to be coated. Sometimes the sphincters are relaxed, causing in- 
continence of urine and faeces. Just before death the bodily emaciation 
is apt to be extreme. 

Obviously we have here two fairly well marked sets of symptoms, 
the mental and the somatic. The latter are not known to be the direct 
results of the former under any other circumstances, though the for- 
mer are frequently caused by the latter. Therefore it would seem to- 
be a fair conclusion to draw that a profound toxic condition underlies 
the disease and is the cause of both sets of symptoms. 

Diagnosis. — Typical cases of Bell's mania do not: give much 
trouble in diagnosis. The febrile condition, the wild delirium with re- 
missions, the hallucinations, the extreme motility, the rapid course,. 
intense emaciation and somatic symptoms are characteristic. In sim- 
ple mania there are no somatic symptoms, very little febrile disturbance, 
if any, and the ideas are more systematized and coherent. In delirium 
tremens there is a clear history of alcoholism, much gastric disturbance* 



THE NON-NEURONIC DISEASES 877 

peculiar visual hallucinations and a general and marked asthenia. A 
meningitis is accompanied by more or less nuchal rigidity and opistho- 
tonos, pupillary symptoms, motor spasm and paresis, vomiting, con- 
tinuous high fever, absence of complete remissions, Kernig's sign and 
the tdchc <ccrebralc. The delirium of typhoid fever or pneumonia can 
be determined by other symptoms present than those of the brain. 
With post-epileptic mania there has been a previous history of epileptic 
attacks and the fatality is much more swift. 

Prognosis. — This is decidedly bad. Spitzka says that recovery 
never occurs, which is the opinion of most authors. This prognosis of 
course applies to the typical cases of the fulminant type, cases in which 
the brain is overwhelmed with the virulent intoxication and leaves no 
changes of an anatomical character discoverable post mortem. There 
are authors, however, who do not consider the prognosis so absolutely 
bad. It is evident that they are including in their statistics the non- 
typical, less virulent cases which recover, or which die at a much later 
period and reveal signs of a diffuse inflammatory process. In the 
words of Pritchard, "the prognosis in the non-organic cases is sta- 
tistically worse than in the organic." How analogous is all this to the 
history of Landry's paralysis ! 

Treatment. — The treatment is not satisfactory. The indications 
are to support the patient's strength, eliminate the toxin and quiet the 
nervous excitement. 

To remove the cause as expeditiously as possible is the first obliga- 
tion imposed upon the attendant. Free diuresis, purgation and dia- 
phoresis should be instituted. Osier says he has been criticised for 
recommending venesection, but yet he repeats the recommendation. It 
seems to me commendable in robust, sthenic cases. Such vascular 
agents as ergot, quinine, etc., have been tried and found wanting. The 
slowness of their action would seem to suggest their uselessness in this 
disease. After the venesection in plethoric cases, the transfusion o\ 
blood or saline solution would be a proper proceeding. To quiet the 
nervous system the straight jacket, with complete isolation and forced 
feeding, has been proposed. Some cases may be quieted with the cold 
bath or the cold pack. Morphia, hyoscine, chloroform, the bromides. 
trional, all in heroic doses, may be experimented with, but will fre- 
quently give negative results. Serum therapy is suggested by the 
probable etiology and pathology of the disease. 

CEREBRAL SYPHILIS. 

Syphilis exerts its baleful influence upon the nervous system direct- 
ly and indirectly. The bacillus and its toxins by their continued action 
produce lesions within the nervous apparatus (organic syphilis of the 
nervous system) or disturb the physio-chemical and consequent func 
tional characteristics of the nervous elements (functional syphilis 
the nervous system). On the other hand, they somehow so affect 
certain parts of the nervous tissue that long after the) have ceased t-. 
be active this tissue undergoes a steady, progressive and character 
istically degenerative change. The former are the true syphilitic difl 



878 THE NON-NEURONIC DISEASES 

eases of the nervous system, the latter are the so-called parasyphilitic 
diseases. It is but fair to say that there is some doubt as to the ex- 
istence of the functional group of syphilitic diseases. Some think that 
they are but the early manifestations of what later on will unmask itself 
as true, organic syphilitic trouble, the functional symptoms being due 
to irritation from the organic lesions, or as true parasyphilitic disease, 
the functional symptoms here being caused by the early disturbance 
in the nutrition of the cellular elements prior to their degeneration. If 
that be so, a view which I am inclined to accept, then there are, strictly 
speaking, no functional diseases of the nervous system of syphilitic 
origin. There are only the organic diseases, or true syphilis, and the 
parasyphilitic diseases. The epilepsies, chorea, neurasthenia, hysteria 
and hystero-neurasthenia, noted by Fournier and others, are but early 
manifestations of either the syphilitic or parasyphilitic troubles. 

Organic syphilitic disease is an affection of the entire nervous 
system. In other words, the majority of the cases of organic syphilitic 
disease reveal symptoms sooner or later that show implication of the 
brain, spinal cord and peripheral nerves. Pure brain syphilis or pure 
spinal syphilis is comparatively rare. Nevertheless in about two-thirds 
of the cases or more, the predominant symptoms are so markedly 
intracranial or intraspinal or neural, that for the sake of practical 
convenience we speak of brain syphilis, spinal syphilis and nerve 
syphilis. Under the present heading I will discuss only brain syphilis. 

Paradoxical as it may sound, it is none the less true that organic 
syphilitic disease of the nervous apparatus is, strictly speaking, not a 
nervous disease at all. It is a disease of the blood vessels and the 
nervous elements suffer because of their close proximity to these dis- 
eased organs and because of their dependence upon them for their 
nutrition. The process in the blood vessels is that of an inflammation, 
a specific arteritis. It may remain confined to the walls of the blood 
vessels and the nervous elements may suffer from the ischaemia caused 
by the narrowing of the inflamed vessels, their complete occlusion, or 
from the presence of a thrombus or embolus within them. If the inflam- 
mation produces, as it usually does, a more or less profuse specific 
exudation, then a gummatous condition and multiple gummatous 
tumors develop. The commonest distribution of this gummatous vas- 
cular inflammation is in the membranes of the base and vertex ; under- 
lying the frequent gummatous meningitis. Syphilitic disease of the 
coats of the blood vessels, eventuating in gummatous meningitis on the 
one hand and in obstructive and other circulatory disturbances within 
the brain substance on the other hand, is practically the basic patho- 
logical process underlying all forms of organic cerebral syphilis. There 
are variations upon these two general forms of pathological findings. 
There may be combinations of the two ; one or the other may be pre- 
dominant ; secondary complications may occur ; and finally the gum- 
matous condition may be diffuse and membranous-like, or it may simu- 
late single or multiple tumors. Whatever the variation be, in its last 
analysis it will be seen to originate primarily in a specific inflammation 
of the blood vessels. This fact is a most important one to bear in mind, 



THE NON-NEURONIC DISEASES 879 

for it explains the great multiplicity, variability and instability of the 
individual symptoms of brain syphilis. 

Etiology. — Syphilis, whether it be the germ, as in all probability 
it is a true germ disease, or the toxin elaborated by the germ, is the 
cause of the vascular disease constituting the basic lesion of brain 
syphilis. This sounds like a truism, but the necessity for repeating it 
is provoked by those cases in which an honest denial of specific infec- 
tion is made. Many times the early somatic signs of syphilis are so 
slight and evanescent that they are completely overlooked and forgot- 
ten. At other times they disappear so rapidly during a brief course of 
mercurialization, and remain away so completely after the medication 
has been stopped, that a false notion of being cured is engendered in the 
mind of the patient and he denies that syphilis can possibly be in any 
way the cause of his present trouble. The larger number of cases of 
brain syphilis that I have seen have presented just such an early his- 
tory. It is in the class of cases in which the primaries and secondaries 
are slight as well as too briefly treated, that tertiary syphilis is so 
likely to occur ; and so emphatically am I convinced of this that when 
I have, upon the examination of the patient, formed a reasonably con- 
clusive opinion that he has brain syphilis, his denial of all early signs. 
coupled with an admission of exposure, clinches the diagnosis and 
makes it positive. 

By referring to syphilis of the brain as tertiary syphilis, it is not 
intended to convey the idea that the brain may not be attacked in the 
secondary stage, or even earlier in the disease. On the other ban.!, 
this form of tertiary syphilis may not occur until many years after the 
appearance of the primary lesion. The larger number of eases appear 
about two or three years after. The recorded limits in which brain 
troubles of this kind may occur after infection are from a tew months 
to thirty or more years. It may even follow hereditary syphilis. The 
term tertiary has no relation, therefore, to the time ni the manifesta- 
tion; it is merely a convenient way of indicating the character and 
location of the lesion. 

Not all syphilitics become the victims of brain syphilis. It would 
seem logical to look for the cause of this in the condition of the nervous 
system rather than in the character of the specific virus. So litt! 
known about the matter, however, that little beyond speculation can lie 
advanced. Certain exhausting influences, such as excessive venery, 
mental wear and tear, dissipation, lack of sleep, alcoholism and trau- 
mata, do seem to determine to a certain extent an outbreak of brain 
syphilis in those who have been infected. An inherited neuropathic 
tendency favors the parasyphilitic rather than this form of the dis< 
An inherited weakness of the circulatory and visceral organs, a familial 
tendency toward arteritis, nephritis, cardiac and hepatic troubles, ma\ 
predispose to brain disorders in a syphilitic. 

Pathology AND PATHOGENESIS. — The most common form of brain 
syphilis is, without doubt, basal gummatous meningitis. Thi 
usually in the subarchnoid space in the vicinity of the optic chia 
and spreads out over the base and up the sides of the brain and down 
between the crura. It causes the membrane to be thickened, opaque 



880 THE NON-NEURONIC DISEASES 

and gummy, and to be covered with numerous knob-like, round eleva- 
tions or tumors, varying in size from a pea or hazel-nut to a walnut. 
These gummata may surround the neighboring cranial nerves, espe- 
cially the optic, the ocular and the abducens. Sometimes the nerves 
themselves are not injured ; usually, however, they appear swollen, 
enlarged, grayish or yellowish white on section with atrophy of the 
nerve-fibres. Both the small and large arteries of the base of the 
brain are involved. Their walls are thickened, and their calibre is 
diminished or occluded. The basilar artery shows this tendency par- 
ticularly. As its terminal branches are so often obstructed, there will 







FIGURE 


197. 










./» 


^3%: 




tk 






ji&. ■ 








L, ^ 










^:: ; -, 












■ 


\ 




4 






/. 


vi 












, \ 


^ 




^~— 







Syphilitic basilar meningitis and multiple gummata at the base of the brain. 
(After Siemerling.) 

be observed numerous foci of softening. Sometimes the remains of 
old hemorrhages are found. Instead of foci of softening there may 
be a diffuse softening over a large area. This basal gummatous menin- 
gitis may assume almost any form and mode of extension. It may be 
associated with a circumscribed gumma. A disseminated extension 
may take place in the form of yellow or gray plaques (meningo- 
encephalitic foci) or in the form of multiple tumors. Even miliary 
gummata are now and then seen. This same gummatous meningitis 
may appear on the convexity of the brain either as a separate process 
or along with the basal disease. As a rule it is less severe on the vertex 
than it is at the base. Yet with this meningitis the underlying cortex 
may be involved (syphilitic meningo-encephalitis), disturbing to a 
profound degree the cerebral functions and by extension into the 



THE XOX-XEUkOXIC DISEASES 



88 1 



depths of the brain tissue, causing a widespread softening, even of a 
whole hemisphere. Simple gummata within the substance of the brain 
are very rare. A gummatous neuritis of the cranial nerves may occur 
separately and apart from any implication of the brain or its meninges ; 

FIGURE 198. 




Syphilitic arteritis of the middle cerebral artery. 
Syph. Syphilitic new growth. 
/. Lumen of the artery. 
mf. Original fenestrated membrane. 
m. Muscular coat. 
a. Infiltrated adventitia. 
sb. Infiltrated subarachnoid space. 
cb. Upper surface of the brain. 
cl. Round cells. 
Cp. Newly formed capillary. 
/>. Pigment. 



(After Heubner.) 



and not infrequently the brain will remain intact whih- many of its 
arteries show syphilitic arteritis. It is composed of a cellular, highl) 
vascular granulation tissue. It is never or rarely purulent, though in 
spots it may be caseated or fibrous. A round-cell proliferation extends 
directly along the adventitia of the blood vessels and also along the 
epineurium of the nerves. Between the bundles of the nerve fibres the 
thickened and infiltrated epineurium sends its pi everywh 



882 THE NON-NEURONIC DISEASES 

like connective-tissue septa. The nerve itself thus becomes swollen, 
while the individual fibres undergo atrophy- 
In hereditary cerebral syphilis the lesions are not unlike those of 
the acquired form, though probably less intense. To sum up, the 
lesions of both hereditary and original brain syphilis involve the 
lymphatics, capillaries, veins and arteries. Endarteritis is the lesion 
par excellence. This may involve the dura or the pia, more especially 
the latter. A gummatous new-growth is formed, and as a result dural 
and pial gummata with gummatous leptomeningitis are seen. Focal 
and diffuse encephalitis with hemorrhages, necrobiosis from obstructive 
disease of the arteries and veins, and fibroid indurations from chronic 
vascular disease are all liable to occur. The wide extent, variable 
character and changeable nature of these pathological findings make 
clear the reason of the great diversity, variability and swift changes in 
the symptomatology of brain syphilis. 

Symptoms. — I sometimes teach that among organic diseases the 
clinical picture of brain syphilis is the homologue of hysteria among 
the psychoneuroses. Brain syphilis has such a wide range of symp- 
toms that it can simulate almost every other known form of cerebral 
disease. Somewhat like hysteria, its symptoms are remarkable for their 
appearance and disappearance, their transference from one part of the 
body to another and their involvement of all known functions of the 
nervous apparatus, sensory, motor, vasomotor and trophic. As the 
entire encephalon is liable to the disease, and as the disease process 
(soft and easily broken-down gummata, hemorrhage, emboli, etc.) 
itself is so inconstant in its minute manifestations, one can readily com- 
prehend how the symptoms or outward signs of these changing and 
shifting pathological phenomena should also be changing and shifting. 
It would be quite an impossible, or at least an herculean, task 
to attempt to classify the symptoms of brain syphilis. And yet there 
is a certain constancy and uniformity in their appearance and group- 
ing, so that after a time one comes quickly to recognize the clinical pic- 
ture as being more or less characteristic. 

Certain distinctive features belong to the symptoms in such a way 
that we can group them somewhat. The symptoms indicative of cen- 
tral irritation are quite distinguishable from those indicative of de- 
struction of the central nervous tissue. Sometimes these two classes 
of symptoms exist simultaneously in different parts of the nervous 
distribution ; at other times one or the other set alone predominate. 
Usually they exist in the same parts, the irritative being followed by 
the destructive signs. Epilepsies and stupor, delirious and comatose 
states, paresthesia and hypaesthesia, spasms and pareses, all thus alter- 
nate or occur together in the same patient or follow one another with 
remarkable persistency. 

Again, the symptoms may be subdivided into those that are due 
to the gummatous meningitis involving the gray matter of the cortex 
and the basal nerves in the irritative and destructive process, and 
those that have to be attributed to the closure of the circulation by 
thrombotic and embolic obstructions or to minute hemorrhages and 
inflammatory foci. The former are apt to be more focal and localized 



THE NON-NEUR0N1C DISEASES 883 

in character and implicate special nerves and individual functions ; the 
latter are rather hemiplegic in character and are diffuse., spreading: 
over segments of the body known to the patient's mind and not in ac- 
cordance with distinct anatomico-physiological arrangements of the 
peripheral neuromuscular apparatus. All this great variability and 
wide extent of the symptomatology of brain syphilis are features that 
are almost pathognomonic of the disease. And yet. as I have tried to 
emphasize before, in spite of all this diversity in the details of the 
symptomatology, in its general manifestation there is a remarkable 
constancy, uniformity and individuality. 

I will now discuss the clinical picture of the commonest form of 
brain syphilis, basal gummatous meningitis. It must not be assumed 
that in these cases the disease is limited entirely to the membranes and 
vessels of the base. In fact, in these basal cases there is practically 
always some disease of the convexity and some neuritis of the cranial 
nerve roots. In the clinical picture, however, the symptoms of the 
basal meningitis predominate. These indicate irritation, compression 
and destruction of the neighboring nervous elements. Foremost among 
the general symptoms is headache. This is characteristic and peculiar. 
The pain is more or less generalized over the whole head, is paroxysmal 
and generally exacerbates with great severity at night. Sometimes it 
resembles the indefinite, indistinct, paresthetic sort of a headache com- 
plained of by neurasthenics ; at other times it is sharp, cutting and 
boring. It is rarely unilateral like hemicrania ; it is less definitely 
localized than the headache of cerebral tumor and abscess ; it lacks 
the dependence upon mental states like the clavus of hysteria ; and it is 
influenced by the stomach, the eyes and other sources of peripheral irri- 
tation which sometimes provoke pain in the head. It is not accom- 
panied by fever as a rule, though sometimes the temperature rises in 
cerebral syphilis. It is a sortr^of a cross between the headache of brain 
tumor and acute infective states; not as wearing and constant as the 
former ; more intense, definite and paroxysmal than the latter. / 'omit- 
ing and vertigo are frequent accompaniments of the cephalalgia. Con- 
vulsions of a generalized character, with unconsciousness, occur in 
periodical attacks. Between these there may be a progressive stupor 
as in all forms of progressive intracranial growths. Weakness of mem- 
ory, failure of intellect and power of attention, and general mental 
apathy are not uncommon. Even dementia of the true type may occur. 
In the midst of all this gradual obliteration of the consciousness, out- 
bursts of mania, severe attacks of excitation, delirium alternating with 
coma may be SO severe a- to require the incarceration of tin- patient ui- 
an asylum. The characteristic changeability of the symptomatology 
brain syphilis is shown in the occasional alteration of these mental! 
manifestations with periods of apparent mental restoration to health; 
The coma may recede, only to return again, however. It is obvious 
that the gummatous meningitic exudation is the cause of these symp- 
toms largely by the intracranial pressure it causes and the encephalitis 
it lights up. Doubtless the same explanation will answer for the 
casional polydipsia and polyuria that are seen in this form of brain. 



884 THE NON-NEURONIC DISEASES 

syphilis. Tubercular meningitis of the base is easily differentiated by 
its general development and more or less elevated temperature. 

Most important are the symptoms dependent upon compression 
and destruction of the cranial nerve roots. The optic and oculomotor 
nerves are the most frequently implicated, usually somewhat more on 
one side than the other. The patheticus and abducens nerves are the 
next most frequently involved, but they are apt to be affected on one 
side or the other only. The fifth, seventh, eighth, ninth, tenth, elev- 
enth and twelfth nerves, as well as the olfactory, are all liable to be 
.affected, but with decreasing frequency in the order in which they are 
enumerated. Optic nerve trouble is particularly common, which for 
the purpose of diagnosis is fortunate. The ophthalmoscope, together 
with an examination of the vision, shows in most all cases some de- 
gree of atrophy. Typical choked disc and neuritic atrophy, with 
neuro-retinitis, are frequently seen on one or both sides. I have seen 
cases, on the other hand, in which the eye ground symptoms were prac- 
tically negative though the visual loss was certain. 

Almost every variety of visual disturbance may be met with, as, 
for example, bitemporal or homonymous hemianopsia ; amaurosis on 
one side with hemianopsia on the other, ultimately becoming bilateral 
amaurosis, which is not persistent as a rule, or complete. The visual 
field, when the optic nerve itself is diseased, may show an irregular, 
concentric contraction, decrease of central visual acuity, etc. All of 
these optic nerve symptoms, exclusive of the atrophy, show a remark- 
able degree of changeability and unsteadiness. The outlines of the 
contracted visual field may change from day to day ; the amaurosis 
may swiftly vary or change from one eye to the other ; the bitemporal 
hemianopsia may be of the most fugitive type. 

Paralytic symptoms, involving all or a part of the third nerve, 
are early and frequent. Ptosis on one or both sides is often seen. 
Sometimes one branch of the nerve gives way after another until the 
whole nerve is involved. Oppenheim declares, however, that a pure 
ophthalmoplegia, interior and exterior, is rare in basal syphilis. 

With involvement of the olfactory roots there results anosmia, 
which may be double or one-sided. 

I have several times seen the fifth nerve involved. This most fre- 
quently occurs on one side and may give rise to hyperesthesia, anaes- 
thesia or rather hypsesthesia of the face, with weakness in the move- 
ments of the lower jaw. The taste is disturbed on the anterior two- 
thirds of the tongue, and there is often a neuroparalytic keratitis on 
the same side. Hearing is affected by involvement of the auditory 
nerve ; at times the irritation produces most annoying tinnitus. When 
the facial is included, the paralysis resembles the peripheral type of 
Bell's palsy, without the involvement of the palate, the hearing and 
the taste. In other words, the paralysis partakes of the nature of a 
peripheral palsy, without, however, alteration in the electrical reactions. 
Facial diplegia occurs. 

The cranial nerve symptoms, various and scattered and change- 
able as they may be, are so constant a constituent of the clinical pic- 
ture of basal gummatous meningitis, that without them the diagnosis 



THE NON-NEUKONIC DISEASES 885 

should be made with much hesitancy. It may be that for some brief 
period in its course basal gummatous meningitis may exist and pro- 
duce other symptoms than those showing implication of the cranial 
nerves, especially the optic and oculomotorius, but such cases must 
be exceedingly rare and such a clinical manifestation would probably 
be very brief. I have never seen either. 

\\ nen the gummatous meningitis is limited to the convexity of 
the brain of course the cranial nerves escape. Moreover, the symp- 
toms are quite dissimilar to those of basal disease. The headache seems 
to be more superficial and localized. Percussion on the outside of the 
skull will elicit sensitive spots or areas, especially above and behind 
the ear and in the occipital region. When the disease process is of 
wide extent, spreading over a large area, there will be epileptiform 
manifestations, convulsions, muscular Iremblings and slight muscular 
rigidity. If the motor region of the cortex is pressed upon by the 
gummata, aphasic manifestations or Jacksonian epileptic attacks, fol- 
lowed by monoplegia, will make their apearance. Eye symptoms, 
like choked disc may not be present until the disease is far advanced. 
Sometimes the motor and sensory disturbances will be of a very marked 
character on the opposite side of the body, such as cpilcptoid attacks, 
tremor, contracture and pai)is. In some cases the mind is affected by 
the associated involvement of the gray cortex. If the meningitis 
focal and scattered in character, the symptoms may be of a focal char- 
acter, depending upon the part of the brain and its localization func- 
tion, pressed upon. In this way occipital meningitis may produce 
hemianopsia, temporary disturbances of hearing, peripheral pains and 
other sensory phenomena. 

In the larger number of cases of brain syphilis these two forms of 
meningitis, that of the base and that of the convexity, occur together, 
though for a time one or the- other seems to predominate. Along with 
the meningitic symptoms are those which may be regarded as in a 
way secondary to the disease in the isolated vessels. In the larger 
vessels, especially those of the base, like the basilar artery and its 
branches, an endarteritis is the particular form of lesion present, while 
in the smaller and terminal capillaries of the cortex it is more of the 
nature of a periarteritis. In these cases thrombi form and emboli float 
off and occlude the circulation: or the thickening of the arterial walls 
brings about almost the same result by the narrowing of the calibre 
of the vessels. The location and size of the artery thus affected 
will of course determine the character of the symptoms, but these will 
partake of the nature of those of an encephalomalacia. When the 
softening is at the base, the great symptom is a p>. hemipL 

which, however, may come and go, first in the leg. then the arm and 
finally the face, several times before- it becomes permanent. The 

and mental functions as a rule remain intact. Premonitory indi- 
cations, like twitching, often precede the hemiplegic attack: on the 
other hand, the parah sis may conic on most unexpectedly and p 
away entirely in a few hours or days. 1 saw a case where tin- patienl 
had to take to his bed. and yet the next day lie was walking around 
almost as well as if nothing had happened. Speech \ ted, hut 



886 THE NON-NEURONIC DISEASES 

there was no loss of consciousness. This hemiplegia is, of course, on 
the opposite side from that on which the affected artery rests. As 
Oppenheim well points out, the laws of localization for crossed hemi- 
plegia (superior and inferior) must be used with some caution in 
brain syphilis. 

Oculomotor paralysis of one side, and hemiplegia of the other, 
are here sometimes caused, not by a focal peduncular disease, but by 
the very conditions of the basal meningitic process. Involvement of 
the basilar and vertebral arteries give rise to pontile and bulbar symp- 
toms. When the arteries higher up are thus obstructed, the well- 
known apoplectic manifestations occur, such as prodromes followed 
by extensive hemiplegia, hemianesthesia, aphasia, hemianopsia. The 
syphilitic nature of these attacks is indicated by the headache and ver- 
tigo that long precede them, by the fugitive character of the apoplecti- 
form outbreaks, the stupor, mental confusion, and dementia that follow 
them. 

With these forms of brain syphilis, especially with the basal type, 
there is often conjoined syphilitic menin go-myelitis. The latter dis- 
ease, as a separate affection, will receive special attention under the 
general head of spinal syphilis. Here, however, a few words must 
be said in regard to the symptomatology of the combined diseases, com- 
monly referred to as cerebrospinal syphilitic meningitis. As a rule the 
brain symptoms stand out in overwhelming prominence. If a thorough 
search be made, however, a fugitive girdle pain, a tendency to para- 
plegic phenomena, irritability of the bladder, localized spinal root pains 
with vasomotor and trophic disturbances, and loss of one or both 
patella reflexes will be discovered. Later on these spinal symptoms 
may become more obvious and more constant. In some cases they may 
even obscure somewhat the cerebral symptoms. Almost any type of 
spinal syphilis may thus present itself with brain syphilis, the more 
common of which are Erb's type of syphilitic spinal paralysis, multiple 
sclerosis, Brown-Sequard's syndrome or Oppenheim's syphilitic pseudo- 
tabes which is not unlike tabes dorsalis in many respects. 

Closely related, pathologically and symptomatically, to this 
cerebrospinal syphilis is the multiple syphilitic neuritis of the nerve- 
roots of Kahler. There is nothing distinctive about this to call for 
special consideration except the fact that the paralysis of the various 
cranial and spinal nerves comes on insidiously and irregularly, and that 
the trouble may readily be mistaken for a peripheral neuritis. Oppen- 
heim says, anent this multiple syphilitic neuritis of Kahler, that it is 
just a little too schematic, a remark which I am inclined to apply to 
the former's own separate description of basilar and vortex forms of 
brain syphilis as though they were separate and distinct diseases. To 
be sure they each have a striking characteristic symptomatology and 
prognosis, but that is the result merely of the location of the disease 
process. To found a classification thus of the same disease upon a mere 
difference of location, is confusing. Especially is this true where, as 
in brain syphilis, the disease process so often occupies both and even 
all localities simultaneously. 

The symptoms do not materially differ in brain disease when the 



THE XOX -NEURONIC DISEASES 88,7 

syphilis is inherited from those in which it is acquired. Occurring thus 
early in life, however, it is obvious why many mental defects and 
epilepsy should be so much more prominent than they are in the ac- 
quired form. 

Diagnosis. — It is easy to confuse brain syphilis with other dis- 
eases when there is not a clear history of infection. The wide extent 
of its pathology and consequent symptomatology account for this and 
the great changeability and transitoriness of many of its clinical phe- 
nomena. As the error is more often committed of attributing a non- 
syphilitic disease to syphilis than vice versa, the differential diagnosis 
is best considered under the headings of the diseases that are thus more 
likely to be mistaken. 

Prognosis. — The prognosis of brain syphilis, both as to life and 
as to permanent disability, depends very largely upon the location of 
the disease process. When it is most active at the base of the brain 
the prognosis is worse than when it is spread over the convexity. In 
neither form, however, is it absolutely unfavorable. Life is endangered 
the more the process approaches and affects the great vital centers in 
the pons and medulla. Involvement of the basilar artery and its 
branches is, therefore, a particularly unfortunate event. This i- 
especially in old age, and when the general health is below par. 

When hemiplegia occurs it may clear up, and later on many re- 
lapses follow. A hemiplegia, however, is always a bad sign, as it in- 
dicates both an advanced and wide state of disease. If the hemiplegia 
does not recede, and especially if contractures have begun, recover) 
is no more to be expected than in a hemiplegia of any other sort. 

In regard to the question of recovery. Gowers has stated that 
syphilis is practically an incurable disease, though he probably would 
not deny that by treatment its symptoms may be suppressed and its 
destructive influence held in abeyance. With this view I am in per- 
fect accord. Therefore it follows that recovery under treatment 
called recovery — can only be looked for when the tissue changes are 
strictly specific and have not gone on to complete degeneration, reor 
ganization, etc. An optic neuritis, for instance, is amenable t<> treat- 
ment, but an optic atrophy is not; a specific meningo-encephalitis m;i\ 
be made to clear up, whereas a necrobiosis due to an arte 
rial obliteration will not give any response to the most heroic medica 
tion. This is the reason that antisyphilitic treatment gives Mich vai i.t 
ble results in cases treated promiscuously and consecutively. 

Treatment. — The prophylactic treatmenl of brain syphilis 
should include the education of the young a- to the dangers of infec 
tion and the heroic treatment of the infection at once a fur it has been 
acquired. Xo half measures are permissible here. A thorough course 
of mercury for a long period, with now and then intervals o\ a tew 
weeks' rest, should be carried out. It is m) own practice to recom 
mend treatment of this sort for a period of not (ess than three years, 
and sometimes many years more. The mereurv may he given by the 
stomach or by inunction. I prefer the latter method myself, \bout 
a dram of unguentum hydrargyri is rubbed int.. the skin d.iih 
every other day, for a couple of weeks, and then a few w ' is 



888 THE NON-NEURONIC DISEASES 

allowed or the mercury is continued in milder dosage by the mouth. 
It is best to use the ointment alternately on the inner side of first one 
arm, then the other, or on the inner side of one thigh and then the 
other, taking twenty minutes or half an hour to rub it in, and covering 
the part afterwards with a bandage. During this mercurialization the 
diet must be attended to, excluding all acids and stimulants ; the exer- 
cise must be regulated and the use of free bathing to promote the ac- 
tivity of the skin must be enjoined. A chlorate of potash mouth wash 
(about 5 per cent, strength) if used often during the day will prevent 
stomatitis. In a few cases even the most vigorous early treatment 
after the above manner, fails to prevent the disease attacking the brain 
or the trouble itself from relapsing. When either of these unfortunate 
events occur, the treatment must be at once renewed and conducted to 
the very point of ptyalism. It is the patient's only hope of avoiding 
the frightful ravages of the disease in the wav of the paralyses, etc. 

In some cases the iodide of potash may be employed with or with- 
out the mercury. It shows it's effects, as a rule, sooner than the mer- 
cury but the effects are not so lasting. The dosage of the iodides 
should be much larger than is usually given. I have myself given as 
much as one thousand grains a day. Beginning with twenty or thirty 
grains, well diluted in water and taken after food, three times a day, 
the dose should be rapidly increased daily until two or three hundred 
grains a day are taken. If the remedy .is well diluted, and the stom- 
ach assisted with a little pepsin and nux vomica, there is little danger 
of the manifestations of iodism. In some cases I have had such mani- 
festations disappear after suddenly advancing the dose to a still larger 
amount, say five or six hundred grains a day. The average case will 
hardly need more than about three or four hundred grains a day, con- 
tinued for two or three weeks or longer. I prefer the potassium salt 
to any of the others, and above all to the many iodonucleins and other 
substitutes put upon the market. 

Where atrophy has taken place, destruction of tissue -and sclerotic 
changes have occurred within the nervous tissues, of course no treat- 
ment, however vigorously applied, can be expected to produce any ben- 
eficial results. This is the reason why such varying reports 
are made in the treatment of consecutive cases of brain syphilis. Hem- 
iplegia, contractures, etc., are to be managed here on the same lines as 
when following other general causes. 

When complete, or what is more frequent, partial recovery, is 
obtained, the patient should be warned of the possibility of a relapse 
and told that the best way to avoid such a catastrophe is to lead a 
steady, regular life, to avoid all mental strain and worry, sunstroke. 
traumata, stimulants and excesses of all sorts, especially in eating and 
sexual matters. 

DEMENTIA PARALYTICA. 

Until quite recently this disease was discussed solely in works 
upon insanity. This was on account of the apparent supremacy of its 
psychic manifestations. Since we have learned more about its true 
nature, we find that pathologically and symptomatically it is an organic 






THE NON-NELJRONIC DISEASES 889 

brain disease. While there may be some doubt as to the strict appli- 
cability of the name chronic diffuse meningoencephalitis, some still 
regarding the disease-process as primarily one of degeneration rather 
than inflammation, there can be no doubt as to the positive changes in 
the cortex and their relationship not only to the psychic but to the 
motor and other equally important symptoms. Hence it is proper to 
now discuss general paresis or dementia paralytica under the head of 
diseases of the brain. The old name progressive paralysis of the in- 
sane ought to be entirely dropped as it represents a conception of the 
trouble not at all in consonance with what we know about it to-day. 

Etiology. — In a few cases a neuropathic heredity can be traced 
but only in a few. The male sex fall victims to it much more fre- 
quently than the female. It occurs most commonly in the middle 
period of life, between the ages of thirty and fifty. It has been seen 
in childhood. It is very rare in old age. Nationality seems to have 
no deterring influence for or against it. It is on the increase every- 
where where the excitements and struggles of life are at their maxi- 
mum. In the cities and the crowded centers of civilization and in those 
walks of life where ambition to get ahead, mental strain, anxieties 
and hopes are the keenest. Nascent races, like the negro, when placed 
under these conditions become subject to it. Fournier ranks general 
paresis along with tabes dorsalis as a parasyphilitic disease. In from 
70 to 90 per cent, of all cases a history of syphilis is obtainable. Like 
tabes it is regarded not as a syphilitic disease but rather as a sequel 
of or the remains after the syphilitic storm. Pathologically and clin- 
ically locomotor ataxia and dementia paralytica are certainly closely 
related. The difficulty of inoculating paretics with the syphilitic virus, 
as shown by Krafft-Ebbing, is a strong point in favor of the syphilitic 
theory of the disease. Acquired and congenital syphilis has been 
traced in some of the cases -seen in childhood. It is probably this in- 
fection, together with the strain and dissipation that lurk behind gen- 
eral paresis, that determine such factors in the etiology of it noted 
above in connection with sex, age, etc. In a happy epigram Krafft- 
Ebbing has summed up the etiology of the disease as covered by "civil- 
ization and syphilization." The particular truth concealed in this 
aphorism is that neither the syphilis nor the civilization alone is likely 
to give ri'se to the disease. The predisposing influence of the former 
and the exciting tendencies of the latter must cooperate. And yet one 
cannot elicit evidence of syphilis in ever} case. ( Hher predisposing 
factors must be assumed in its place by those who are not yet ready t«» 
accept the dictum that all paretics arc syphilized. In two instances in 
which the infection was strenuously denied, and in whom I could not 
obtain the slightest evidence either in the past or present histor) of the 
disease, typical dementia paralytica developed so., 11 after the residence 
of the patient was transferred from tin- countr) to the city. In both 
instances the new life was most strenuous, full of trouble and anxietj 
and wanting in either happiness < »r contentment. Nothing beyond a 
neuropathic heredity could be discovered as a predisposing cause. It 
is not unreasonable to suppose that in a certain -mall percent 
cases there may be such a congenital weakness, such a want "i vital 



89O THE NON-NEURONIC DISEASES 

capacity, in certain of the central neurones that when subjected to 
the sudden and unwonted strain of competitive civilization they suc- 
cumb. 

Pathology and Pathogenesis. — The principal pathological 
changes are observed in the cerebrum, though there are changes often 
in the spinal cord also. 

Macroscopically the brain is smaller, smoother and harder than 
normal. There is an atrophic condition of the convolutions, making 
the gyri smaller and flatter and the sulci less deep. This is most no- 
ticeable in the frontal and parietal regions, though it may be seen also 
in the island of Reil and in the temporal convolutions. It is sugges- 
tive of cortical degeneration. The membranes are frequently adher- 
ent to the brain and when torn away often peel off spots of cortical 
substance with them. The pia is thickened and clouded while the 
dura looks as though there had been an internal hemorrhagic pachy- 
meningitis. There is an excess of cerebrospinal fluid and a variable 
degree of internal hydrocephalus with distention of the ventricles and 
granulation of their walls. 

The weight of the entire brain is diminished and when it is cut 
into it feels firm and cheesy. The borderlines of the gray matter are 
less sharply marked than normal and the thickness of the cortex is 
seen to be decidedly lessened. The degree of sclerosis varies in differ- 
ent cases. The white matter is also affected but not as much as the 
gray, being firmer in consistency and seemingly more compact. Areas 
of softening, old hemorrhagic remains and arterio-sclerosis are not un- 
frequently observed. In a word the gross appearances are such as we 
might expect from a prolonged inflammatory, degenerative, sclerotic 
process. 

The microscopic appearances are striking and quite typical though 
the nature of the process underlying these appearances is not clear. 
The cells of the cortex are more or less atrophied and the neuroglia 
and interstitial tissue is hardened and increased. The ganglion cells are 
variously altered, the nuclei and fibres of the neuroglia are increased, 
the spider cells are proliferated, the bloodvessels are hyaline and col- 
loid, and sclerosed, and the lymph tracts are dilated and displaced. Ac- 
cording to Tuczek the medulated tangential fibres of the upper cor- 
tex, especially of the frontal lobe and island, are degenerated. The 
whole condition, as Wernicke expresses it, suggests a chronic progres- 
sive process of the disease in the cortex that causes an ultimate atro- 
phy of its constituent parenchymatous elements. 

Similar appearances are sometimes observed in the basal ganglia, 
and gray matter of the crura, pons and medulla. The pyramidal and 
posterior tracts may also be implicated. It is not known whether the 
degeneration of the pyramidal tracts is primary or secondary. That 
of the posterior tracts is probably primary due to the same cause that 
produces the cerebral changes. The optic nerves, and occasionally some 
of the other cranial nerves, are wasted. Even the peripheral cutaneous 
nerves are now and then degenerated. 

It will be noted that this pathological picture brings to mind very 
forcibly the pathological picture of tabes dorsalis, the only difference 



THE NON-NEURONIC DISEASES 89 c 

being the location of the primary focus of the disease. Fournier him- 
self suggests that the two affections are but different expressions of 
the one and same morbid entity, possibly the one and same disease. 
Clinically it has long been remarked that locomotor ataxia often ter- 
minates in dementia paralytica and that paretic dements not in fre- 
quently develop tabes dorsalis. 

The question of the nature of the primary process in the patho- 
genesis of the malady is quite as unsettled here as it is in locomtor 
ataxia. There are strong contestants for the primary degenerative 
theory on the one hand, and for the meningeal inflammatory theory on 
the other. It is highly probable that whichever view is ultimately 
proved to be correct, it will apply to both dementia paralytica and loco- 
motor ataxia alike. 

Following the lead of Fournier many still maintain that as a more 
•or less remote result of the specific infection a primary degeneration 
takes place in the cortical cells and their processes, with a secondary 
sclerosis and inflammation in the interstitial tissues and cerebral mem- 
branes. Many facts seem to lend credence to this view and none more 
so than the one overwhelming fact that in the true syphilitic diseases 
of the central nervous system, which are distinctly meningeal and 
inflammatory no such characteristic changes are produced as are ob- 
served in dementia paralytica. The arteritis, gummata and gumma- 
tous meningitis of cerebral syphilis are never seen in these degenera- 
tive diseases, while on the other hand the characteristic degenerative 
appearances of the latter do not seem to occur with the inflammatory 
processes of cerebral syphilis. Either there must be two distinct forms 
of inflammation resulting from syphilis, the degenerative and the or- 
dinary, or the two processes must be distinct and separate. In the 
light of modern pathology the latter seems to me to be the only answer 
to the question. The primary inflammatory processes of syphilis of 
the central nervous system, whether immediate or remote, are not the 
same as the degenerative results of syphilis as seen in dementia para- 
lytica and tabes dorsalis. 

Those who contend that the disease is primarily inflammatory with 
the parenchymatous atrophy as a secondary result are tending back to 
the old view of a primary sclerosis, though they place the initial stages 
of the disease process in the cerebral meninges. This is somewhat in 
line with Obersteiner and Redlich's explanation of locomotor ataxia 
•on the basis of a particular form of spinal meningitis. Bevan Lewis 
partly sums up this view by stating that there are three Ma^'s in the 
cortical process: (1) the stage of inflammatory change in the tui 
adventitia of the arteries: (2) tin stage of hyper-development of the 
lymph-connective system of the brain, with degeneration ami disap 
pearance of the nerve elements and the axis-cylinders; and I 3 > tin- 
stage of general fibrillation with shrinkage- and extreme atroph) of 
the parts involved. In perfect consonance with this view the disc 
is sometimes called chronic diffuse meningoencephalitis. 

Whether the meningitis is an initial, synchronous or terminal phe 
nomenon with the encephalitis or not. the primary inflammator) na 
ture of the entire process is the essential feature of this view. If tins 



892 THE NON-NEURONIC DISEASES 

be so we are at once confronted by the question as to the nature of 
the process in the similar disease, locomotor ataxia. If the two dis- 
eases are the same then primary inflammation, it would naturally be 
supposed, underlies the pathology of the latter. Many declare that 
it does but that it originates in the membranes. These theorists prob- 
ably then also believe that dementia paralytica originates in a chronic 
meningeal inflammation. Why discuss either disease then outside of 
the chapter or chapters devoted to cerebral and spinal meningitis ? The 
degenerative sequelae can then be easily treated of in a special para- 
graph and emphasized as one of the many results of these special 
forms of meningitis. If, however, the meningitis is not the primary 
source of the trouble, though it is still affirmed that the process is 
primarily an interstitial inflammation, then it is presumably the same 
in locomotor ataxia, and we are back to the old posterior spinal sclero- 
sis theory in which the degeneration was affirmed to be a secondary 
process. The only way of escape from this dilemma, it seems to me, 
is to deny completely the relationship between the two diseases, tabes 
dorsalis and dementia paralytica, and that we cannot do. 

The whole question is in need of more light, though for the 
present we are justified, in my opinion, in regarding the primary pro- 
cess as a degenerative one in the nervous elements in both diseases. 
This degeneration is the result of an exciting cause acting upon a nerv- 
ous system predisposed by syphilis. Secondary to the degeneration are 
the interstitial sclerosis, meningeal inflammation, and other vascular 
alterations. 

Symptoms. — It goes without saying that the most prominent 
symptoms of dementia paralytica are the mental exhibitions. For this 
reason the disease was formerly named and classified among the pure 
psychoses. Prominence and importance are not synonymous terms. 
There are other symptoms so important that were they absent, the 
mental symptoms would lose much of their significance as signs of 
this affection. The diagnosis should never be positively based upon 
the psychic symptoms, though they may furnish the strongest clue 
to the trouble. In every case search should be made for the motor 
signs, evidences of apoplectiform attacks, speech disturbances and 
Argyll-Robertson pupils. One or more of these will usually be found 
and when associated with the psychic exhibitions, the diagnosis of 
the organic cerebral disease, dementia paralytica, is assured. 

The special value that attaches to the menial change is that it be- 
gins to show itself so early that it almost assumes the role of a prod- 
rome and awakens a strong suspicion before any of the other symptoms 
can be clearly detected. The panorama of the psychic disturbances 
moves through the successive stages of gradual excitable dementia. A 
steady down grade in the intelligence, with a weakening of its chan- 
nels of expression, the judgment and conscience and morale, is the 
psychic side of the clinical picture. Those mental powers, with the 
high obligations that accompany them, which have been the last to 
have been laboriously evolved during long periods of evolutionary de- 
velopment in the race and in the individual, like the apex of a pyra- 
mid, are the first to topple. There is a gradual descent from manliness 



THE NON-NEURONIC DISEASES 893 

to childishness, from altruism to egoism, from a high sense of obliga- 
tion to a low sense of responsibility. While the memory, the imagina- 
tion and the will may be affected, it is the intelligence, the comparing 
and relating faculty, that is especially damaged. *As this faculty ex- 
ercises an inhibitory control in health over all of the lower faculties 
of the animal personality, the more it is weakened the more the lower 
faculties and their personality come to the front. This explains the 
egoism, the selfishness, the shamelessness, the cunning, the unreason- 
able scheming, the emotionalism, the instability, unreliability and irri- 
tability, the abnormal ideomotor excitement, almost resembling mania, 
the expansive imaginativeness with its hallucinations and delusions, 
its volubility, loquaciousness and general bustling activity and self- 
satisfaction usually seen in these patients. The guiding reins of the 
intelligence have fallen and the steeds of the lower faculties are run- 
ning away. Only exhaustion brings them to a standstill in the ter- 
minal dementia. The whole picture is a sort of psychic analogue of 
spastic paralysis, or a failure of pneumogastric inhibition over the ac- 
tion of the heart. 

So fine are these psychic changes in the beginning that often they 
are not noticed except by the closest observers and the nearest 0/ 
kin. There is a tendency towards indifference to business, home ties 
and obligations of honor. The individual is not as scrupulous about 
little matters, his dress, his word, his promises, his speech, his en- 
gagements as he has been wont to be. He is a little impatient ni re- 
straint and seems to seek his own comfort and pleasure more deter- 
minedly. He becomes fickle and frivolous. He neglects his wife and 
children upon the slightest selfish whim. He grows inattentive and 
forgetful. He makes use of language and performs acts that are un- 
called for, unaccountable and often shameless. At times he is em- 
barrassingly indelicate, vulgar, cynical, obscene. He seems to have 
lost, as the disease advances, all sense of the proprieties, all finer ap- 
preciation of his proper relationship to the world outside of himself. 
He will expose his person, urinate or defecate upon the highway. 
utterly indifferent of publicity. This general apathy and indifference 
coupled with the unbridled egoism often brings him in conflict with 
his partners and associates in business, in opposition to those who are 
most interested in his welfare, and even in actual struggle with the 
law. Thus irritabilities at home and lawsuits abroad are his portion. 
Sharpers and tricksters observing and taking advantage <>f* his weak 
ness, often lead him into concocting vast schemes, spending vast sums 
of money, starting huge industrial undertakings, developing unwieldy 
financial combinations which help to enrich them but invariably spell 
ruin and disgrace for him. Who knows what financial crash* >. in- 
dustrial upheavals and great business failures have not been the legit- 
imate ending of the grand schemes of some unrecognized but irre 
sponsible paretic dement ! More disrupted family circles, more thiei 
erv in the world of high finance, more immorality, dishonesty, and 
general devilishness of a certain order may be due to incipient general 
paresis than we are willing to admit. 

Not only on the side of moral apathy and ethical indifference i 



894 THE N0N- NEURONIC DISEASES 

dementia paralytica exhibit itself but also on that of positive self- 
satisfaction, unceasing activity, restlessness and excitement. The 
calm egotism and self-satisfaction of these patients is sometimes posi- 
tively exasperating. They know it all, they are absolutely impervious 
to instruction. They are therefore often apparently happy and pleased 
with the world, themselves and things in general. Their restlessness 
may exhibit itself in many ways ; in taking long walks, scribbling whole 
reams of paper, inventing a lot of useless gewgaws or perambulating 
about the house all night. The environment of such patients is in a 
constant state of turmoil. Those about him become worn out with 
his incessant volubility and his constant bustling without achievement, 
involuntarily irritate and cross him and drive his weak, irritable dis- 
position into frequent explosions of terrific anger. Though danger- 
ous at times, these passionate outbreaks are not lasting. Sometimes 
they are most violent and provoked by the most trivial circumstances. 

Loss of memory is characteristic of almost every case. It must 
not be confused with the mere apparent loss of memory caused by 
the overwhelming force of the selfishness. One of my patients was 
given some money by her husband, who was a poor man, to go out 
and pay some grocery and other bills in the neighborhood. She soon 
walked in with nineteen shirtwaists, to purchase which she had used 
all the money and declared she had forgotten all about the shop-bills 
which she still held in her hand. In the true amnesia, recent events 
are more easily forgotten than remote. If the patient is asked to 
describe his life he will be very loquacious about his early years but 
very chary in reporting what he did the week before. Inability for 
mental computation is particularly noticeable. A previous lightning 
calculator will struggle over the addition or multiplication mentally of 
a column of two figures. Amnesia is probably at the basis of this 
trouble. 

With the steady progression of the disease the signs of psychic 
irritability and intellectual weakness become more and more pro- 
nounced. They assume the character of grandiose hallucinations and 
delusions, particularly in regard to himself. On account of this folic 
de grandeur he identifies himself with kings, presidents and mighty 
geniuses. It is a favorite occupation with these poor creatures to 
pose as the reincarnated Messiah. Sometimes they imagine they are 
veritable Monte Cristos with unlimited wealth. The paretic dement 
is always a great artist, an inexhaustible inventor, a poet of world- 
wide renown, an astute detective and the scientist of scientists. While 
he does not hold long to these various poses, sometimes he does dabble 
in the work of the particular character he imagines he is. The vacuity 
of all his efforts and absolute nothingness of the sum total is at all 
times pathetic if not amusing. 

Instead of the feeling of well-being there is sometimes one of de- 
pression. Hypochondriasis or melancholia may occur early in the 
disease, though even these usually assume the grandiose, lie is a 
Byronic sufferer on account of the cruelty of the world. The torments 
ol Dante's Inferno are nothing in comparison to what one of my pa- 
tients declared he endured. Thev fancy thev are the victims of most 



THE NON-NEURQNIG DISEASES 895 

extraordinary anatomical and physiological conditions. A man told 
me once that the food he ate flew out of the top of his head up against 
the ceiling. Unique, astonishing, surpassingly strange though sad and 
depressing are these delusions, and thus they are in keeping with the 
general psychic manifestations of the disease. As the excitement, 
volubility, and psychic irritability approach their climax the patient be- 
comes dangerous and more and more intolerable. He bursts out in 
passion, screams, rushes about, seizes those near him, scolds and pours 
forth a volume of senseless words and phrases and makes all sorts 
of strange and wild grimaces. The oncoming exhaustion soon shows 
itself in beginning bodily emaciation, especially as the patient refuses 
all nourishment, in a more prompt appearance of the condition of tire. 
in lessened volubility, in increasing inattention and dullness and finally 
in absolute stupor and dementia. The end is then not far off. 

Among the non-mental somatic symptoms of the disease the ear- 
liest to appear, and therefore of the greatest importance, are the 
Argyll-Robertson pupil, pupillary inequality y tremor, especially of the 
tongue and lips, special disturbances of the speech and alterations of 
the handwriting. These may be present when the mental manifesta- 
tions are quite elusive. Others may precede the mental and all other 
symptoms by months and years. They are never entirely absent when 
the mental symptoms are noticeably prominent. They should always 
be strenuously sought for and constitute the stronger foundation for 
the diagnosis of the disease in the entire complexus of symptoms. De- 
mentia paralytica is an organic disease with positive somatic representa- 
tion. The prominent psychosis that constitutes a part of its clinical pic- 
ture is the direct result of the organic damage in the cerebral cortical 
elements. It is not entirely and wholly an insanity in the usual mean- 
ing of the word. 

Pupillary rigidity to light stimulation, with preservation of re- 
sponse to accommodation, the Argyll-Robertson pupil, is an early - 
of general paresis. It is estimated that it occurs in si\t\ per cent. <>t" 
the cases. It may precede all other symptoms and be the only one 
present for many months and even several years, h is usually a con- 
tracted pupil; some ophthalmologists say always a contracted pupil. 
Mydriasis may exist, however, in some cases. It is usually bilateral. 
though it may be more marked in one eye than in the other, <>r ma\ be 
entirely unilateral. The pupils are sometimes unequal or irregularly 
contracted. Hippus has been observed. The vision is more or less 
disturbed and on account of the occasional headache with scintillat- 
ing scotomata the disease for a time has been mistaken for lu-mi- 
crania. Double vision from paralysis <»!" the external ocular nuts 
and even paralysis of accommodation have been rarel\ noted among 
the earlier manifestations. These eye symptoms, and others it will be 
remarked, are much like those sometimes seen in the preataxic si 
of locomotor ataxia. For a while in seme cases tin- distinction l><-tv, 
the two diseases cannot be made. 

Soon a peculiar, fine, fibrillary tremor announces itself. li i^ 
especially noticeable in tin- sides and tip of the tongue and in the lips. 
When the patient talks it can aK<» be slightly detected. It may be i 



896 THE NON-NEURONIC DISEASES 

fined to certain muscles or it may appear in every part of the body. 
It shows itself when the patient write's and it is seen in the hand and 
foot sometimes when they are held out. The oscillations are small, 
rapid and sometimes accompanied by jerky movements. Together 
with and partly on account of the tremor and fine incoordination, the 
patient's speech and writing are strikingly characteristic. The former 
is slow, blurred, drawling, stumbling and interrupted. There seems to 
be difficulty in getting the words out and consequently delay and hesi- 
tancy. Syllables and parts of whole phrases may be omitted or slid 
over indistinctly. There is no distinct scanning of the speech, but 
rather uncertainty, jerkiness and irregularity. In the articulation the 
lips tremble and shake markedly, unusual parts of the face are worked 
and a nasal tone is assumed. Generally ordinary language will do to 
exemplify these manifestations. I sometimes demonstrate them more 
forcibly by getting the patient to repeat, as well as he can some such 
phrases as these : Peter Piper picked a peck of pickled peppers ; round 
the rugged rock the ragged rascal ran ; buy baby blue bottle of black- 
berry brandy, etc. Familiar, semi-automatic speech, like reciting the 
multiplication table, can usually be uttered with more facility than 
speech requiring constant attention and thought. The latter is always 
accompanied by a greater slowness of diction, partly on account of the 
growing dementia. In reading it is apt to be more noticeable than it is 
in automatic speech, but not quite so marked as in thoughtful conversa- 
tion. The same general features seen in the speech trouble are seen in 
the handwriting. There is tremulousness, jerkiness, irregularity, slow- 
ness, laborious effort, repetitions and omissions. Incoordination and 
dementia are behind these. Sometimes there is absolute want of sense, 
coherency and relevancy in what is penned. Paralexia or irrelevant 
reading has been noted in some cases. If the patient has been a letter 
writer, always ask to see some of the earlier letters. In some cases 
there may be detected slight occasional lapses, both of thought and 
diction, that now show themselves so prominently. As in all examina- 
tions of this sort, involving the patient's intelligence and education, the 
previous culture must be known and taken carefully into consideration. 
A man of mere ignorance may attempt to write and the product bear 
somewhat a resemblance to that put forth by an incipient paretic. 

So important are the speech and writing defects in the diagnosis 
of the disease that their examination must never be omitted, however 
slight the other symptoms may appear. They alone are almost path- 
ognomonic and can ofttimes be detected by special examination when 
otherwise they would not attract attention. 

A history of temporary syncope and paralytic attacks is extremely 
suggestive. These may be either apoplectiform or epileptiform. 
Without warning and without apparent immediate cause, the patient 
suddenly has a sinking spell with more or less coma and muscular 
weakness. He may turn pale and fall, or he may remain stationary in 
a sort of petit mal state. On the other hand, he may have all the indi- 
cations of a true apoplectic seizure; sudden unconsciousness, a fall, 
relaxed extremities with flushing of the face, stertorous respiration, 
rapid heart action, elevation of temperature and death. Hemiplegia. 



THE NON-NEURONIC DISEASES 897 

monoplegia, aphasia and all the usual accompaniments and sequelae 
of cerebral hemorrhage and obstruction may appear in some cases. 
Usually these attacks are of the temporary type and sooner or later 
the patient is almost back to his old condition. The paralysis and the 
aphasia may be very brief and Meeting or they may be partially per- 
sistent. The phenomenon repeats itself, varying in time and location. 
True epileptic-like seizures, generalized and partial, usually without 
aurae, are perhaps more common than apoplectic strokes. Sometimes 
these precede the appearance of any of the other typical symptoms. 
All forms of epilepsy may be simulated by them, even the psychic and 
the status types. After these paralytic and epileptic attacks the pa- 
tient's general mental condition, speech, etc., are apt to be worse. 

In the cases that are hemiplegic the gait is characteristic, pains are 
absent and the reflexes of the knee are exaggerated. In some cases, 
however, there will appear, if not at first, then later on, loss of the 
knee-jerks, static and motor ataxia, lancinating pains and other sensory 
phenomena without much motor weakness. These, of course, are the 
manifestations of tabes dorsalis. They may appear before the mental 
indications of dementia paralytica ; in about eighty per cent, of cases 
they come on after them. Even perforating ulcer, arthropathies, bed 
sores, optic atrophy and other vasomotor and trophic conditions obtain 
late in the disease. With involvement of the pyramidal tracts together 
with the posterior, a combined spinal degenerative sclerosis with its 
usual clinical picture will be associated with the general paresis. 

So extensive is the clinical portrayal of the disease at times that 
one may well be in doubt as to what are the symptoms of the funda- 
mental malady and what the symptoms of the complications. There- 
is ground evidently for the contention of Fournier that the entire 
complexus of symptoms, cerebral and spinal, represents one uniform, 
wide disease of the entire nervous system, with its maximum repre- 
sentation, and usually limitation, in the sensory path. 

Diagnosis. — In the earlier stages the diagnosis of dementia 
paralytica is very difficult and this is the time when a correct diagtt 
is especially desirable. To save the patient, his family and his property 
a prompt recognition of the first signs of the trouble should be within 
the ability of every physician. A later diagnosis is neither especiall) 
brilliant or useful. By that time the patient is apt to In- so far ad 
vanced that no possible treatment will be of any benefit and so obstrep 
erous that the family will already have thought n\ putting him in con 
finement. Be very suspicious, therefore, when a strong, industrious, 
devoted man suddenly begins to neglect his engagements, his family 
and his usual duties; when he loses his power of concentration and 
attention; when his apperceptions become clouded and his judgments 
confused; when trifling causes excite him abnormally ; when lie dallies 
and delays and seems to want initiative force; when he i^ easil) 
wearied mentally and physically; when he lets loose in his sexual life 
is immoral, obscene and indifferent to all law and order; when h< 
unwarrantably egotistic, self-satisfied and selfish, or, on the other hand, 
is melancholy and hypochondriacal. 

If a history of syphilis can he obtained in addition t<» these mani- 



898 



THE NON-NEURONIC DISEASES 



festations in a man whose temperament is not of the neurotic type, 
the suspicion is strengthened. Ask to see some of his letters and note 
any changes in their style, both as to writing and contents. Especially 
look out for irrelevancy of phraseology, repetition and omission of 
words and syllables. Note his surprise when his attention is called 

FIGURE 199. 





General Paresis with arthropathies. (After Lloyd.) 

to these things, showing that they were done absent-mindedly, as it 
were. Search keenly for the somatic signs, such as the Argyll-Robert- 
son or other pupillary defect, the tremor, the speech disturbance. 

In the early stage the disease most liable to be confused with 
general paresis is neurasthenia. Very often these patients are neu- 
rasthenic and hysterical; it therefore behooves the examiner to be all 



THE NON-NEURONIC DISEASES 899 

the more careful to detect the presence of the dementia and other signs 
of the trouble. The somatic symptoms are rarely liable to be mis- 
taken for signs of neurasthenia, certainly not the pupillary changes 
In nervous exhaustion there may be a kind of aphasia or a tremulous- 
ness, but there are none of the paralytic attacks of an apoplectiform 
or epileptiform character. 

In hysteria the latter may be simulated, but there are sensory phe- 
nomena as well as absence of the peculiar tremor that determine the 
latter. In neither neurasthenia nor hysteria is there that strange and 
almost weird-like absence of the old personality in the midst of all 
the bustling activity and garrulousness. Something seems to have 
dropped out of the mental life of the man that represents not so much 
a loss of force as a loss of control. In neurasthenia, and much more 
so in hysteria, the personality may be somewhat changed, but it is a 
more radical change ; nothing is lost, but everything is altered. In 
general paresis there is a distinct hiatus in the mental picture, and 
that which has left the vacancy is missed because of the absence of 
its controlling force over the entire man, mental and physical. The 
paretic dement does not, except in very rare cases, worry about his 
condition. He is not introspective or the victim of phobias and fixed 
ideas, as a neurasthenic or hysteric is. He is objectively egotistic, while 
the latter are subjectively egotistic. The paretic dement has the ego- 
tism o-f a child, selfish, grasping, indifferent to others, happy when its 
wants are supplied, enraged when subjected to restraint. The neu- 
rasthenic and the hysteric, to a lesser degree, has the egotism of the 
intense introspectionist. The former is then usually gay and exhilar- 
ated, the latter are more apt to be sad and whining and depressed. 

This difference between the general mental states of dementia 
paralytica and neurasthenia or hystero-neurasthenia, coupled on either 
hand with the other special symptoms of the two sets of diseases, ought 
to aid very materially in the making of the differential diagnosis. 

The paroxysmal character of the headache in hemicrania, its 
abrupt onset and cessation, the aurae, the peculiar eye symptoms and 
the absence of the typical psychosis of general paresis, will distinguish 
the former from the latter. And yet there are eases of the latter in 
which there are only headache and neurasthenic manifestations early in 
the disease, just as in some cases of hemierania. In even the- 
however, the headache does not come and go periodically, localize itself 
closely, and be associated with vomiting as in migraine. 

Tumor has been mistaken for early dementia paralytica. There 
are headache, neurasthenic symptoms, sometimes aphasia, epileptiform 
seizures and mental changes in tumor, but there are also choked disc, 
absence of tremor, absence of Argyll-Robertson pupil and none of the 
characteristic mental exhibitions. Mental Stupor and slow pulse are the 
traits of an intracranial neoplasm. 

Gutnmata and gummatous meningitis may cause symptoms that 
closely resemble those of dementia paralytica. And this is not 
markable when it is remembered that the arteriosclerosis and menu 
encephalitis set up by syphilis may conceivably provoke the d. 

five changes in the nervous elements that are observed in tli 



900 THE NON-NEURONTC DISEASES 

syphilitic troubles. In cerebral syphilis there is a sharper localization 
of the symptoms and more of an inflammatory irritative character 
about them than there is in general paresis. The headache is distinct 
and sharply localized, the paretic symptoms are comparatively limited 
and the somatic signs are more pronounced than the mental, whereas 
in general paresis it is the other way. Argyll-Robertson pupil, tremor, 
speech difficulty such as are seen so frequently in paretic dementia 
are not traits of cerebral syphilis, but, on the other hand, ocular palsies, 
monoplegias, sharp epileptic seizures are more to be expected in the 
latter. In late cerebral syphilis, particularly of the vertex type, quite a 
typical form of general paresis may supervene; but by that time the 
essential nature of the disease will have been well established. 

Multiple sclerosis can be differentiated without much difficulty. 
The mental symptoms when present are of the stuporous or mildly de- 
lirious type, not so unique and sui genesis as they are in general paresis. 
Nystagmus, scanning speech, intentional tremor, paresis with some 
rigidity, ocular palsies with diplopia of a transient character, will help 
to easily distinguish a disseminated sclerosis. 

Senile dementia is a disease of old age and is not abrupt, but is 
clearly a condition running parallel with a slow wasting of the entire 
organism. It has not the more prominent somatic signs of general 
paresis. 

Subacute and chronic alcoholism produce an exhilaration, a 
weakening of the higher controlling mental faculties and mild delirium 
that in some respects brings to mind dementia paralytica. Tremor, 
speech troubles, restlessness, insomnia, loquacity, amnesia, belong to 
both diseases. In some of the cases of alcoholism that I have seen I 
have suggested the diagnosis of incipient alcoholic meningo-enceph- 
litis. Here, however, the irritative traits of the psychosis have seemed 
to me to be more pronounced than they are in general paresis. There 
are illusions and hallucinations and other typical phenomena that are 
rarely met with in the latter disease. The etiology of the trouble is 
almost quite obvious and to a large extent helps to determine the 
diagnosis, just as it does in the encephalopathy of lead poisoning and 
bromine, trional and other forms of drug intoxication. 

Prognosis. — This is absolutely bad. Most cases die in about 
three years, others have lived to eight and ten years. It has been re- 
ported that two or three cures have occurred. The only cases tha; 
hold out any possible hope of recovery are those that are recognized 
early, give a clear history of recent syphilitic infection and undergo 
vigorous antisyphilitic treatment. Death is caused by exhaustion, 
hypostatic pneumonia, bedsores, genito-urinary complications or other 
intercurrent trouble. As partial remissions in the course of the dis- 
ease sometimes occur, it is imperative to warn the relatives not to mis- 
take these for a cure. 

Treatment. — A paretic dement is always a nuisance and dan- 
ger to himself and his family. The proper place for him therefore' is 
in a sanitarium or asylum. Here he will be given careful nursing, 
plain, nourishing food and such occupation and diversion as will keep 
him out of harm's way and in the least excited state of mind. Tonics 



THE NON-NEURONIC DISEASES 0,01 

may be employed on general principles but medicinally the only hope- 
ful treatment is the specific. Large doses of the iodides should be 
given a trial. If they show the slightest tendency to do harm, they 
should be withdrawn at once. Temporary remissions sometimes fos- 
tered by this treatment are mistaken for cures. Early in the disease- 
some improvement may follow massage, hydrotherapy and gentle ex- 
ercise. Xo severe measures of any sort should be attempted. Cold 
to the head may allay excitement. Other symptomatic measures in- 
clude the bromides for the insomnia and epileptic seizures, hypoder- 
mics of morphine, hyoscine, duboisine and ergotin for the delirious 
excitement, the usual measures for the apoplectiform attacks and forci- 
ble feeding for the refusal to take food. 

MULTIPLE SCLEROSIS. DISSEMINATED SCLEROSIS. 
CEREBROSPINAL MULTIPLE SCLEROSIS. 

This is a chronic, progressive malady of the cerebrospinal axis, 
occurring in the early part of adult life and notable for the wide 
diversity of its symptoms. While in the typical forms of the disease 
there is a certain degree of uniformity in its clinical picture, in many 
of the atypical forms it closely simulates a large number of other 
nervous diseases, from which it is sometimes extremely difficult to 
differentiate it. On account of the disseminated nature and wide 
distribution of the lesion, with the consequent variability and wide 
diversity in its clinical manifestations, a concise definition of multiple 
cerebrospinal sclerosis cannot be satisfactorily formulated. When con- 
fronted with a suspected case, the diagnostician must keep well in 
mind the nature of the lesion and apply most carefully his knowledge 
of nervous physiology and localization. 

Etiology. — Multiple sclerosis is almost unique in being the only 
chronic progressive organic disease that occurs so early in life. The 
vast majority of the cases make their appearance between the a 
of twenty and thirty years. It rarely occurs before fourteen, and still 
more rarely after fifty. Cases have been reported in infancy. In old 
age it is practically unknown. Young male adults are rather more 
frequently afflicted than females. Neither climate, race nor season 
enter into its etiology. 

Heredity in some instances has seemed to have played a minor 
role in the transmission of a neuropathic condition. Eichhorsl -aw 
it in an eight-month's child whose mother was a victim of the dis© 

An inherited degeneracy rather than a mere neuropathic state may 
underly some of these cases. There is now under my observation a 
man, thirty-two years of age. who exhibit- and gives a typical hi- 
tory of disseminated sclerosis, which began about eight years 
His family history is remarkably suggestive. IN- grandparents on 
the paternal side were first cousins. Mis father, an uncle, and an 
aunt, were born deaf-mutes. I lis mother became a deaf-mute in child- 
hood after a severe attack of scarlet fever. The patient himseli 
the younger and weaker of twins. Mi- twin brother and one Other 

brother are apparently perfect in every way. There can be discovered 



902 THE NON-NEURONIC DISEASES 

no exciting cause whatever for the onset of the trouble. He has been 
temperate and has led an even, comfortable life. He was married 
over ten years ago and has two healthy daughters. 

Infection is the preeminent cause of multiple sclerosis. This is 
so true and it so frequently follows the infectious fevers that it may 
almost be called a post-infectious disease. This undoubtedly explains 
in part many of the other etiological factors of the disease, such as 
the age of the patient, sex, slight hereditary influence, etc. Typhoid 
fever and malaria seem to be the more frequent infections that pre- 
cede it. Variola, scarlet fever, measles, pneumonia, whooping-cough, 
diphtheria, cholera, influenza, erysipelas and acute articular rheuma- 
tism, has each seemed to have borne a causal relationship to it. It 
is not the result of syphilis. The disseminated form of spinal syphilis, 
with its multiple foci, is another disease. The puerperium has been 
followed by it and so has dysentery. Oppenheim believes that intox- 
ication from metals is sometimes the origin of the trouble and declares 
he has observed it follow carbonic dioxide poisoning. Gerhardt traced 
it to mercurial intoxication in one case. 

Trauma, shock and sunstroke are doubtful causes. It is probable 
that infection underlies these alleged causes. In some cases it is 
difficult to assign any cause for the disease. 

Pathology and Pathogenesis. — The gross appearance of the 
cerebrospinal axis in a case of multiple sclerosis is unique and striking. 
Even before the removal of the soft membranes, the glistening, hard, 
sclerotic foci may be seen irregularly scattered through the white 
matter of the cord and brain. These nodules vary, from 1-25 of an 
inch to an inch in size ; are irregular in shape ; and are harder than 
the surrounding tissue, though not so hard as connective tissue. There 
is no uniformity in their distribution. They are found most commonly 
in the w r hite matter of the centrum semiovale, internal capsule, crura 
cerebri, pons, medulla and columns of the cord. They are not con- 
fined to any tract or part of a tract. They sometimes involve a quar- 
ter, a half or entire cross-section of the cord. By extension they im- 
plicate the gray matter, though they never seem to originate in the 
gray matter. They are sharply outlined, though the neighboring tis- 
sues may be more or less indurated. This produces a sort of diffuse, 
as well as disseminated, sclerosis in some places. 

Under the microscope these nodules are seen to be fibrous in 
structure with a proliferation of the neuroglia and the other changes 
common in medullary degeneration. They are not connected appa- 
rently with the walls of the bloodvessels, though the latter may be 
proliferated and their walls thickened, distorted and otherwise sugges- 
tive of an inflammatory process. The degeneration is not of the sec- 
ondary type so that by many the disease is supposed to be a primary 
form of sclerogliosis. My own observations lead me to believe that 
some cases are of the nature of a congenital defect, in the same way 
that the cases of syringomyelia and Friedreich's disease are. The 
nature of the lesion, the marked influence of a neuropathic heredity, 
and the frequent absence of all exciting causes are very suggestive. 

Infections produce inflammatory and neuronic degenerative (lis- 



THE XOX-XEUROXIC DISEASES 



903 



orders, but in no other disease do they cause the unique patches seen 
in this disease. Infection probably acts as a prominent exciting cause 
in most cases. 

Running through the nodules may be seen axis cylinders. The 
myelin substance breaks down but the axis cylinders and ganglion cells 
show a great power of resistance to the sclerotic process. It is not 

FIGURE 200. 




Disseminated sclerosis of the brain and the spinal cord. (Partly schematic.) (After Lcyden.) 

probable that the axis-cylinders undergo any regeneration under these 
circumstances. 

The nodules and sclerotic process implicate and surround some- 
times the peripheral nerve-roots and cranial nervi 

The origin of this peculiar form of sclerosis 1- hidden in much 
mystery. The pathological finding- do not give absolute validit) to 
any one explanation, though they are highl 

There are three hypotheses held among the various pathologists. I 
have alreadv mentioned that one authorities hold that the 



904 THE NON-NEURON IC DISEASES 

ease is a primary proliferation of the neuroglia, a sclerogliosis, and 
that many of the other presentations suggestive of inflammation and 
softening are purely secondary to the irritative presence of these 
sclerotic nodules. Other writers state that the pathological process is 
primarily a minute myelomalacia, the result of the presence of minute 
infected emboli. These infected emboli obstruct the circulation in 
the minute terminal bloodvessels of the brain and cord. The tissue 
in spots softens, breaks down and is absorbed. The vacant area is 
then occupied secondarily by the overgrown neuroglia. Still others 
maintain that the sclerosis arises from an inflammatory process com- 
mencing in the arteries. This as well as the preceding explanation 
is in consonance with the infectious nature and origin of the disease 
though many of the later findings do not lend either of them very 
strong support. 

Symptoms. — Two significant facts stand out in the symptomatol- 
ogy of multiple sclerosis, and while beautifully indicative of the char- 
acteristic nature of the lesion, are even of greater importance when it 
comes to the question of diagnosis. The first noteworthy fact is that 
the symptoms, whatever they may be, are rarely if ever complete. The 
paralysis, the anaesthesia, the trophic and mental disturbances, never 
go on to complete paralysis, complete anaesthesia, etc. It is exceedingly 
rare for an entire tract, center or cerebrospinal association to be com- 
pletely severed or obliterated. As a rule some fibres and cells re- 
main intact, and as a result the symptomatology exhibits such general 
characteristics as paresis, paraesthesiae, incoordination, tremor, jerking 
movements. This will be brought out in the further discussion of the 
symptoms. 

The other notable traits about the general symptomatology of 
the disease are the wide diversity and great variety of the individual 
symptoms, showing more or less implication of all parts and all func- 
tions of the cerebrospinal apparatus. This would naturally be looked 
for from such a lesion as multiple sclerosis usually reveals. 

And yet in spite of all this variability and diversity, the symp- 
tomatology of typical multiple sclerosis is singularly definite and uni- 
form. It is this clinical picture that I will now attempt to describe 
and when I have done this, I will point cut the possible variations in 
the picture. 

As a rule the onset of the disease is very insidious. The patient 
first notices a little difficulty in his walking. It seems to be stiff, 
irregular and a trifle jerky. The lower limbs feel zvcak and numb. 
As he has probably come through a severe infectious fever, and has 
been convalescing for several weeks, he attributes this weakness and 
numbness to his lowered health and vitality ; and therefore, he does 
not pay much attention to it at first. lie notices, however, that it 
does not improve but seems to get worse. Moreover he begins to have 
vertiginous attacks, reels slightly and has to take great care lest he 
fall when he turns suddenly. He is becoming cognizant of a slight 
tremor in his limbs, especially when he moves them voluntarily. His 
bladder appears to be weak and he has some trouble retaining his 
urine. All of these manifestations, not unlike the early manifestations 



THE NON-NEURONIC DISEASES 905 

of myelitis, gradually increase, or at least continue unabated, until, 
becoming alarmed, he seeks the advice of a physician. 

A careful examination now reveals a partial paraplegia, spastic m 
type, with muscular rigidity and exaggeration of the reflexes. The 
gait is unsteady and much like that of alcoholic intoxication. It is 
spastic and paretic, incoordinate, ataxic, and trembling. It may reveal 
the characteristics of cerebellar ataxia. The tremor and incoordina- 
tion may be observed in all of the movements of the body, especially 
of the limbs, of the eyes and the muscles of speech and parts under 
the more immediate control of the will. The tremor is absent during 
rest and appears only upon voluntary movement. It has therefore 
been denominated an intentional tremor. At times it accompanies re- 
flex and automatic movements. It is irregular, wobbling and occurs 
in oscillations of five Or six to the second. Sometimes the tremor is 
coarse and choreic in appearance. On this account the patient cannot 
carry a glass of water to his mouth without spilling it, or write, or 
touch promptly the end of his nose. It is impossible for him to walk a 
chalk-line on the floor, climb a ladder, or kick squarely the leg of the 
table. This ataxia is also static in character and the Romberg symp- 
tom is more or less present. 

The muscular stiffness, weakness, ataxia and intentional tremor all 
render the patient exceedingly awkward in all of his movements. The 
head jerks and oscillates, the tongue is protruded in a jerking manner, 
the eyeballs jerk (nystagmus) and the speech is thick, slow and jerk- 
ing (scanni)ig or syllabic). 

With all this muscular disorder and weakness, there is no atrophy 
or changes of electrical reaction. The reflexes arc increased and usually 
an ankle clonus can be easily elicited. 

The sensory symptoms are not of very great significance, except 
those of vision. There may be numbness in the beginning and this 
may go on to a considerable degree of hypaesthesia. Complete anes- 
thesia does not occur, although a hemianesthesia has been reported. 
In such cases there is always some sensation. The ataxia in this dis- 
ease is not the result of the sensory disturbances so much as of the 
motor trouble. Even less frequent than the tactile disturbances are the 
disturbances of the muscular, temperature and pressure senses. Neu- 
ralgic pains are not uncommon and the Brown-Sequard symptom-com- 
plex has been observed. 

A rather striking and confusing characteristic "i' these sensor) 
symptoms is their instability and variability. They are temporary and 
come and go most unexpectedly. In this respect the) bear a resem- 
blance to the symptoms of hysteria and cerebrospinal syphilis. The 
reason for this is obvious. 

The visual symptoms of multiple sclerosis an important and should 
be sought for in every suspected rase. Diplopia occurs as the result <>t 
the involvement of the ocular muscles. In a very large number of 
the cases there is irregular and partial atrophy of the op' \ 

complete atrophy of the nerve is so ran mworth) of fur- 

ther consideration. An ophthalmoscopic examination of the fundi 
shows in most of th< n atrophic pallor of the "titer <>r temporal 



go6 THE NON-NEURONIC DISEASES • 

halves. Spots occur here and there and the two fundi never present 
the same appearance. These fundus changes appear in about twenty 
per cent, of all cases. As a result of these changes in the fundi, the 
optic nerve, and the central neurones that take part in the visual act, 
many symptomatic phenomena occur. The vision becomes blurred 
and misty and may be the first indication to the patient of his trouble. 
This diminution of vision scarcely ever advances to complete blind- 
ness. The Held is irregularly contracted and central scotomata, first 
for colors and then for white, become prominent. Scintillating sco- 
tomata are sometimes present, and sometimes there is simply achroma- 
topsia. Neuritic changes may precede the atrophy and the visual dis- 
turbance is usually the outgrowth of a partial retro-bulbar neuritis of 
one or both eyes. Thus the vision is sometimes markedly impaired 
without any noticeable alterations in the fundi. 

The pupils may be unequal and contracted. Ophthalmoplegia has 
been seen a number of times, though it is rare. 

A very important symptom when it does occur is an apoplecti- 
form attack. There is unconsciousness and hemiplegia, both very tem- 
porary and disappearing in a few hours or days. Sometimes the at- 
tack resembles an epileptic one, at other times it is like a severe stroke 
of apoplexy with prolonged after results. In such cases there is 
marked headache and vertigo. Sometimes the temperature is increased. 

The mental faculties are not usually affected. There may be dull- 
ness, however, hebetude, general apathy, with melancholia and weak- 
ening of the memory. The impulsive laughter is not a mental symp- 
tom. It is entirely involuntary and does not represent in any way a 
mental mood. Sometimes it is paroxysmal and exaggerated, and be- 
ing- frequently repeated greatly annoys the patient. It is exceedingly 
rare for illusions, hallucinations or delirium ever to be present. 

Diagnosis. — The above description represents a more or less 
typical case of multiple sclerosis. Such cases, however, are not the 
ones usually met with. The atypical cases, the aberrant cases, the so- 
called aborted types, the "formes frustes" are the ones that too often 
cause the confusion in diagnosis. Moreover, difficult is it in practic- 
ally all cases to make a diagnosis early in the disease, when an accurate 
diagnosis is especially desirable. 

Practically every case exhibits some approach to the general clin- 
ical picture which I have attempted to outline. Here and there a 
particular symptom may be absent, or the grouping of the symptoms 
may be quite unusual. This is all to be expected when one remembers 
the character and distribution of the lesion. If the symptoms are in- 
tracranial as well as spinal, rather insidious in onset, and slow in 
progress, to a certain extent variable and falling short of completeness, 
and above all suggestive of an interrupting lot of scattered foci within 
the nervous paths, the diagnosis of a disseminated sclerosis is almost 
certainly indicated. 

In the early period of the disease one should be keenly observant 
of the motor zveakness. As this may be the only symptom for many 
weeks or months, it should be closely studied. Its character is that of 
a spastic spinal paralysis. A slight nystagmus, a diplopia, a failure of 



THE NON-NEURONIC DISEASES 907 

eyesight may accompany it. Sooner or later the nystagmus the 
optic atrophy, the dysarthria, the intentional tremor, the vertigo and even 
the temporary apoplectic attacks will announce themselves. Oppen- 
heim saw a unilateral optic atrophy as the only symptom in a case for 
twenty years. I have seen a tremor with merely a little vertigo cause 
a great variety of diagnoses to be made during a period of a year or 
more. In one case that I had under observation for nearly two years 
there were hysterical manifestations with merely a slight ataxia and 
misty vision. The case had been variously diagnosed as hysteria, loco- 
motor ataxia, neurasthenia and epilepsy from a possible incipient intra- 
cranial tumor. It gradually assumed the classical picture of a cerebro- 
spinal disseminated sclerosis. 

Too much caution therefore cannot be exercised in the early 
diagnosis, and it may be put down as an axiom that at this stage a 
positive diagnosis is practically impossible. It cannot be more than a 
strong suspicion. 

The atypical forms of the disease may show every sort of com- 
bination in their symptomatic presentation. The form that resembles 
a progressive spastic spinal paralysis is perhaps the commonest. The 
head symptoms, such as the optic atrophy, the diplopia, the nystagmus 
and the dysarthria, as well as the sensory manifestations, must be 
earnestly sought for and will usually be found, but more or less 
scured by the more prominent spinal symptoms. There is a hemi- 
paretic form that has been referred to by Oppenheim, Charcot. Ed- 
wards, Bickeles and others. A glycosuria, tachycardia and asphyxia 
may indicate a bulbar form. An acute ataxia of the upper extremities 
with bulbar symptoms giving rise to an alternate hemiplegia has been 
observed. 

Among the more common diseases with which insular sclerosis 
may be confused are transverse myelitis, spastic spinal paralysis. I< 
motor ataxia. Friedreich's disease, bulbar paralysis, amyotrophic lateral 
sclerosis, post-infectious disseminated myeloencephalitis, chronic men- 
ingitis, dementia paralytica, apoplexy, epilepsy, paralysis agitans and 
especially hysteria. So large a number of diseases is disseminated 
sclerosis liable to be mistaken for, that sometimes its diagnosis i- best 
made by exclusion. A careful consideration ^\ the clinical picture 
presented by these various simulated affections, therefore, should 
always be borne in mind. The reader is referred t<> their discussii ,;i 
in other parts of the book. A word must be said, however, lure in re 
gard to the differentiation of this disease from spastic spinal para! 
locomotor ataxia, dementia paralytica and hysteria. 

In spastic spinal paralysis the head symptoms, such a- the head 
ache, the optic atrophy, the nystagmus, the scanning speech, an- ab- 
sent. There is no intentional tremor and no ataxia. Th< 
and paretic, but it is not irregular and jerky. There are particularly 
no sensorv or mental alteration-. The muscular atrophy i^ a little i 
marked than in multiple sclerosis, though n<>t so marked a- in anterior 
poliomyelitis, or amyotrophic lateral sclerosis, or progi nuscular 

atrophy. The spasticity, together with the 1 tion of the ki 

jerks, is perhaps a little more pronounced in spastic spinal paral 



908 THE NON-NEURONIC DISEASES 

In multiple sclerosis the rectal, and especially the vesical, functions 
are apt to be somewhat disturbed. 

Locomotor ataxia has been diagnosed from the ataxia which 
sometimes obtains in insular sclerosis. The former is a sensory dis- 
turbance, however ; the latter a motor. In locomotor ataxia Rom- 
berg's static ataxia is promptly manifested when the patient is asked 
to close his eyes while standing. The mere closure of the eyes does 
not so seriously discommode the victim of disseminated sclerosis. The 
absent knee-jerks, the fulgurating pains, the anaesthesia, the Argyll- 
Robertson pupil, the early loss of sexual power and other sensory,, 
degenerative symptoms will help to distinguish tabes. 

Dementia paralytica is a diffuse meningoencephalitis and has 
some symptoms not unlike those of multiple sclerosis in which the 
cerebral symptoms predominate. There is a form of post-infectious 
disseminated myeloencephalitis that cannot be distinguished from mul- 
tiple sclerosis, and sometimes changes into the latter. Dementia 
paralytica can usually be distinguished by the more distinctively mental 
character of some of its symptoms than the mental manifestations of 
multiple sclerosis, though it must be admitted that the differentiation 
at times is extremely difficult, if not impossible. In dementia paralytica 
the growing irritability, the weakening memory, the failure of con- 
tinued attention, the restlessness and excitability, the moral and sex- 
ual indifference, the exaltation of ideas and folie de grandeur, must 
be carefully taken into account. The incoordination and tremor, as 
shown in the penmanship and speech of the paretic dement, are char- 
acteristic. The finer and more complex voluntary movements of the 
hands are very noticeable, as well as the fibrillary tremor of the tongue. 
In multiple sclerosis the tremor and incoordination are much coarser. 
The unequal pupils, the Argyll-Robertson pupil and the absence of nys- 
tagmus characterize general paresis. 

Between no two diseases is a mistake more liable to be made in 
some cases than between multiple sclerosis and hysteria. Every symp- 
tom characteristic of the former may be simulated by the latter. More- 
over the two diseases not infrequently coexist in the same patient. 
When after a most careful examination there is still doubt, it is judi- 
cious for the practitioner to throw the weight of his suspicion on the 
side of the organic disease. In hysteria the temperament of the pa- 
tient, the psychic factors in the etiology, the psychic complexion of the 
entire clinical picture and the exceeding variability and instability of 
the symptoms speak plainly. The sensory manifestations are more pro- 
nounced in hysteria than they are in disseminated sclerosis. In the 
latter the intentional tremor, the optic atrophy, the characteristic dys- 
arthria, the nystagmus and the incoordination are to be closely noted. 
If these symptoms occur in a hysteric, excepting, of course, the optic 
atrophy, they can be made to show slight degrees of alteration by 
some sudden influence upon the patient's mind. It must be admitted 
that at times it is next to impossible to say whether a case is hysterical, 
a case of multiple sclerosis or a combination of the two diseases. I 
have seen a case of multiple sclerosis regarded for several years by 
different diagnosticians as locomotor ataxia, hysterical ataxia and in- 



THE NON-NEURON1C DISEASES 

sanity. Lately I saw a case diagnosed as hypertrophic pachymenin- 
gitis. 

Prognosis. — The prognosis of disseminated sclerosis in regard to 
life is favorable. Only when the disease attacks the vital centers in 
the medulla does it cause death directly. The fatal issue is usually 
brought about by some complication or intercurrent disease. In re- 
gard to ultimate cure, the prognosis is not good. A very few cures 
have been reported. Usually the disease runs a long course of years, 
progressively getting worse, but with occasional intermissions of quies- 
cence, or even partial remissions. Other degenerative and inflamma- 
tory troubles may be lighted up in the course of a multiple sclerosis. 
and the prognosis then becomes the prognosis of this particular disease. 

Treatment. — The treatment is not very satisfactory. Quiet, reg- 
ularity of habits, hygienic environment and all the other recommenda- 
tions for slow, progressive, chronic troubles are here in order. Above 
all avoid severe, radical measures. Why electricity is recommended 
I cannot understand. In my own opinion it had better not be em- 
ployed. Hot and cold baths, stimulants and over-exertion must all 
be prohibited. Special forms of the disease call for special lines of 
treatment. Syphilitic cases should be combated with mercury and the 
iodides. Apoplectic cases, myelitic and encephalitic complications de- 
mand a certain amount of antiphlogistic treatment. Local bleeding with 
leeches may be of some avail in such cases. In all cases the steady use 
of the iodide of potassium is about the best medicinal line i^i treatment 
to be employed. Arsenic, nitrate of silver, quinine and mild hydro- 
therapy, chiefly for their tonic effects, are useful at times. In spite 
of all treatment most of the cases steadily progress, often in an irreg- 
ular manner for many years. 

TUMORS OF THE BRAIN. 

Every variety of tumor attacks the brain, solid, granular and 
tic. In fact, the intracranial structures seem to be a favorite seat for 
new growths, whether they appear elsewhere in the bod) or not. \- 
compared with other organic diseases of the brain the) are not so com- 
mon. They seem from the reports to be more frequent than tumors 
of the spinal cord. They partake of the same characteristics in a gen 
eral way as they do when in other parts of the body. The only thin- 
that makes them of special interest in cerebral patholog) is the effect 
of their presence upon the functions and histological structures of the 
brain itself. Only in some few particulars does their intracranial seal 
cause them to exhibit special differences. For instance, fatty tumors 
are comparatively less frequent in the brain than the) are elsewh 
gliomatous tumors are never found outside of the skull except in the 
retina and spinal cord. It is more common for massive tubercular 
growths to appear in the brain than elsewhere, Aneurism constitutes 
a variety of tumor hut it will be discussed in a section by itself as it 
is more of a disease- of the circulatory apparatus than a new growth. 

Etiology.— There is nothing specially distinctive about the etiol 
Ogy of brain tumors more than what is true of them when located 



9IO THE NON-NEURONIC DISEASES 

elsewhere in the body. Their essential causes are but little known. 
The granulomata, tubercle and syphiloma are, of course, infectious in 
origin; some of the gliomata and fatty tumors owe their existence to 
developmental anomalies and other congenital influences ; echinococci 
and cysticerci are parasitic ; actinomycosis is an infectious form of 
tumor. 

Heredity is supposed to exercise a slight influence in predisposing 
to the tumor itself and its particular variety. Males suffer about twice 
as often as females. This may be due to the greater incidence of cer- 
tain exciting influences in the former than in the latter in some cases 
but certainly not in all. The difference between the sexes in this 
respect varies with the nature of the tumor. It is with sarcomata 
that the sexes approach more nearly to an equality. 

All ages, from six months to advanced years, are subject to brain 
tumor. Certain tumors exhibit a choice of age in their appearance. 
In the first twenty years of life, one-third of all cases occur. The 
relative number diminishes then until it becomes quite small after fifty. 
The reason of this is obvious since the infectious and other conditions 
out of which the tumor is evolved are more common in these years. 
Tuberculous tumors are found most frequently in childhood and early 
adult life, though they may be seen up to old age. Parasitic tumors 
are incidents of early adult years. So also are gummata and gliomata. 
In early and middle life the sarcomata join the gummata and gliomata 
in the frequency of their occurrence. Carcinomata have been diagnosed 
at all ages but most of them have been seen between the ages of forty 
and sixty. The late tumors are the sarcomata, gummata and carcino- 
mata. The rarity of all the other varieties of tumors renders their gen- 
eral etiological characteristics of slight importance. 

Traumata of the head, such as blows and falls, are undoubtedly 
in some instances the excitants of a morbid growth. So also may be 
old cicatrices. In some instances the tumor may have been latent but 
the trauma initiated the secondary disturbances upon which notice- 
able symptoms arose. Hence traumata must not be given too much 
credit for the production of intracranial neoplasms. 

Pathology. — It is difficult to make a perfectly satisfactory classi- 
fication of all the tumors that attack the brain, for our knowledge in 
regard to them is not entirely adequate and they vary in so many par- 
ticulars. Neither their frequency, their location, their causation nor 
their intimate structure will form at present a basis for accurate clas 
sification. They may be enumerated, however, thus: tubercle, syph- 
iloma, glioma, sarcoma, myxoma, carcinoma, fibroma, osteoma, choles- 
teatoma, lipoma, psammoma, neuroma, echinococcus and cystic ere us. 
To these may be added erectile tumors or vascular enlargements, actin 
omycosis, abscesses and cysts due to hemorrhage and encephalomalacia. 
and dermoid cysts, which will not be discussed here. 

Some of these growths may be single or multiple, simple or com- 
plex. They may vary in consistency and intimate appearance in the 
course of their development. A broken down glioma looks not the 
same as an original one. A sarcoma may be limited or diffused over 
a considerable area. A tubercle may be single or multiple. An osteoma 



THE NON-NEURONIC DISEASES 911 

and a fibroma may seem to be amalgamated into an osteofibroma. In 
the same way osteosarcomata, gliosarcomata, angiosarcomata and 
fibrosarcomata may be recorded. 

A tuberculous tumor is usually a single, rounded mass, varying 
in size from that of a nut to that of a hen's tgg or closed fist. These 
tumors are not miliary as they are seen to be in tubercular meningitis 
though rarely the whole brain has been infiltrated with minute miliary 
concretions. They are the most frequent of all the brain tumors and 
are slightly more often located in the cerebellum than in the cerebrum. 
There may be more than one tumor. They are readily detached, as they 
do not infiltrate though they damage somewhat the encircling brain 
tissue. The tumor itself is not vascular, hence when it breaks down 
it exhibits an opaque, cheesy aspect, sometimes softened here and 
there, but not very extensively. Calcification and pus formation are 
among its possible late alterations. It may surround itself with a 
fibroid capsule. Apparently the growth starts in the lymphatic sheath 
of the blood vessels. Vascular obstruction, thrombosis, meningitis, 
cerebral softening and inflammation are among its complications. The 
tubercle bacillus carried to the brain by way of the blood stream is, of 
course, the immediate cause of the morbid development ; hence tuber- 
culosis of the lungs, articulations and other parts of the body is apt 
to be present though not necessarily so. All the usual characters 
of a tubercle, such as the appearance of the cells and the presence of 
the bacilli, belong to these tumors as they do to the same tumors else- 
where. 

Sometimes a syphiloma so closely resembles a tuberculous tumor 
that only the presence of the specific bacillus in the latter enables one 
to distinguish them apart. It varies in size from a pea t<> a walnut 
and is irregular and nodular in shape. Like tubercle it is non-vascular 
and tends strongly to caseation. It does not become purulent like 
tubercle. On section it exhibits scattered, chees) spots separated by 
firm, reddish-gray fibrous tissue. The periphery is irregular, thick 
and grayish with sometimes numerous vessels and evidences of arte- 
ritis. The surrounding brain substance is not infiltrated though it is 
atrophied and otherwise damaged. Old gummata may be BOft and 
broken down though less markedly so than tubercle, or they ma\ 
rear shrunken, fibroid and encased in a capsule. All of the late 
changes are different from those of tubercle and help to differentiate 
the two. In these there is a recognizable connection with the menin 
and a tendency to extend along the surface of the brain in a grayish, 
gelatinous sort of membrane. With these i> often associated a gum- 
matous meningitis; with tubercle there may be a scattered miliar) 
tuberculous condition in the vicinity. Gummata are mosl frequently 
met with in the cerebrum and pons Varolii, rarely in tin cerebellum 
and basal ganglia. Tiny an- superficial and are attached t.. the pia 
mater. Even deep gummata haw their origin from the pia usually. 
Like tubercles they may sometimes ^tart in the dura mater and thence 
invade or only compress the brain. Tin- growth ma 
vascular walls* elsewhere than in the meninges, though 

The sarcomata are among the most interesting and ft' the 



912 THE NON-NEURONIC DISEASES 

brain tumors. They form a large group and on account of their posi- 
tion, combinations and integral changes they assume various modifi- 
cations. They range in size from a nut to a fist. They are of connec- 
tive-tissue origin and therefore start from various tissues. 
They seem particularly to grow from the periphery into 
the cranial cavity. The bones at the base of the skull, for instance, 
the sphenoid, the temporal and the occipital often form their nidus. 
The dura, the periosteum, the other membranes or the brain substance 
itself may be their starting point. They are primary or secondary and 
their internal changes and amalgamations give rise to myxosarcomata, 
gliosarcomata, fibrosarcomata, osteosarcomas, etc. They are of ail 
shapes and may be single or multiple. Rapidly developing, as a rule, 
they are grayish or white in appearance or yellowish according to the 
admixture of cells and bloodvessels. They are harder than gliomata 
as a rule and only occasionally reveal patches of caseation and disinte- 
gration. They are rich in cellular elements, especially round and 
spindle cells. Sometimes they possess an alveolar structure and they 
may even break down into cysts. Pigmentary, calcareous and other 
changes may develop within them. They grow into the cerebral sub- 
stance but are as a rule quite sharply defined from it. They may even 
be encapsulated. As endothelioma they contain endothelial cells from 
the lymphatics. Sometimes they infiltrate without displacing the brain 
substance. Round about them the tissues are destroyed somewhat and 
they are often accompanied by meningitis. A curious condition is a 
diffuse, spread out sarcomatous manifestation in the meninges along 
with the tumor. 

Gliomata are not as frequent as seems to be commonly supposed. 
They are strictly neural tumors and are often due to congenital 
anomalies. They never involve the meninges and bones and usually 
appear in the cerebrum or cerebellum, rarely anywhere else. They de- 
velop out of the neuroglia tissue and so infiltrate the brain substance 
that they can never be shelled out as tubercle can. They range in size 
from a hazel nut to a hen's egg. The largest tumors of the brain are 
the gliomata. In the middle they are reddish-gray or yellowish-white, 
according to their age. Sometimes they look very much like the brain 
tissue itself and have the same consistency. They undergo various 
changes so as to be mucoid or fibrous in character. Especially prone 
are they to disintegrate and being vascular, to exhibit signs of old hem- 
orrhages. Cysts and cavities are liable to form in their center. The 
rapidity of their growth varies and they rarely, if ever, become en- 
capsulated. 

On microscopic examination the typical glia cells, small, spider- 
like cells with delicate, fibrous prolongations are seen, mingled with 
an abundant supply of bloodvessels. The formation of the tumor sug- 
gests strongly an inflammatory process with reactive neurogliosis. 
The tumors are much more easily detected by their appearance when 
situated in the white matter than when in the gray matter of the brain. 

Of course they damage the tissues which they infiltrate though 
sometimes intact fibres will be seen coursing through them. The brain 
is altered in shape and enlarged where they are located. The so-called 



THE XOX-XEUROXIC DISEASES 913 

hypertrophy of the pons, for example, is simply a condition of glioma- 
tous infiltration. It has been confounded with sclerosis of the brain 
and optic neuritis accompanying hemorrhage or softening. The tumor 
is usually single though multiple glioma is a very rare possibility. 

As a primary growth carcinoma of the brain is very rare. Usually 
it is secondary to cancer elsewhere. It is a soft, vascular, irregularly 
outlined growth that partly infiltrates and partly displaces the braia 
tissue. It may spring from the dura and spread out or it may be a 
circumscribed or diffuse neoplasm within the brain in any situation. 
As compared with other tumors it is rather frequent in the central 
ganglia. It is both single and multiple, sometimes symmetrical in 
both hemispheres. Its contents are colloid, consisting of large cells 
sometimes with several nuclei. Wernicke refers to their tendency to 
softening and destruction of all the tissues. 

Fibromata are small, very rare tumors of the brain, occurring 
chiefly in the cerebellum and cerebellar peduncles. They have been 
seen multiple and single. Dana intimates that the enlarged and hard- 
ened pacchionian bodies may be regarded as of the nature of fibromata. 
Calcification in tumors and actual bony tumors occur in the brain and 
may be single or multiple. 

Osteomata or fibro-osteomata usually develop in the dura mater 
and its processes. 

Psammomata are small fibrous growths, filled with calcareous par- 
ticles, that develop in the meninges, pineal gland and choroid plexus. 
They are hemispherical, smooth, hard and gray. They show no marked 
tendency to grow. 

In the hypophysis adenomata may develop and be accompanied by 
acromegalic symptoms. 

Cholcstcatomata or pearly tumors are found sometimes post mor- 
tem at the base of the brain in the recesses of the skull. They are 
composed of epidermoid cells in concentric layers. They give the ap- 
pearance of white, shining nodules and are said to contain cholesterine 
and stearine. Usually they are innocent but at times they develop as 
large as a fist, growing into the cerebral substance'. 

Xcuromata, small growths containing nerve elements, melon- 
omata, lipomata, angiomata, enchondromata, and teratomata, are all 
SO exceedinglv rare as to be unworthy of lengthened consideration. 

Cysts of 'the brain, excluding those due to hemorrhage and sofl 
ening, are parasitic in origin. These arc hydatid or cysticercous. The 
former is usually single and found in tin- cerebral hemispheres, either 
in the ventricles or the white substance Rarel) it has been seen in the 
membranes, the central ganglia, the cms. pons, cerebellum and me- 
dulla. The echinococcus is tin- cause of tin- hydatid cyst Those due 
to the cysticerens cellulosa are- apt t<> be- multiple-, as many as tut;, 
and a hundred cysts having been counted. They are- si.,u in growth 
and are scattered over the- surface- of tin- brain and in the- ve-ntriele-s. 
are encapsulated and provoke no symptoms. It must not be forgotten 
that cysts are sometimes due- to degenerated m-. .plasms, a. is seen so 
frequently in gliomata. 

As an immediate- or remote result ol th< neo 



914 THE NON-NEURONIC DISEASES 

plasm in the intracranium, certain changes are produced in the brain 
and surrounding structures. The gross appearance of the brain is 
altered. There is a flattening of the gyri and an arching out of the 
cortex. This is not noticed when the tumor is cortical or meningeal 
in origin. 

The softening and destruction of the brain substance around the 
tumor have already been referred to. 

Displacements and distortions are effected by the extension of the 
growing mass. Where the space is confined, as beneath the tentorium, 
the displacements, as for instance of the pons by growths in the cere- 
bellum, are sometimes very considerable. On account of the obstruc- 
tion of the passages between the ventricles internal hydrocephalus of- 
ten results. Tumors of the cerebellum and quadrigemina act thus. 
Compression of the venae Galeni which carry the blood away from the 
choroid plexuses is responsible sometimes for the hydrocephalic con- 
dition. Irritation and inflammation, especially in the meninges, is an- 
other effect of the presence of the tumor. And sometimes the cranial 
bones are thinned out, actual perforation having been observed over the 
tympanum. 

x\ll of these secondary results are produced by direct pressure and 
destruction of the growing mass ; sometimes by remote and indirect 
pressure as the result of the foreign body being thus confined within a 
fixed cavity. The choked disc, so-called, and other cranial nerve in- 
juries are the result of compression of the nerve by the growth. In 
children the general intracranial increase of pressure has caused a 
separation of the sutures. In a few instances even spinal cord changes 
have been observed, due possibly to the general increase of pressure 
in the cerebrospinal canal, to nutritive disturbances and to toxic fac- 
tors. 

Symptoms. — The brain is an organ inclosed within unyielding 
walls ; it is a compound organ with special functions belonging to each 
of its constituent parts. A tumor, therefore, will cause two distinct 
sets of symptoms, the general, due to the general increase of intracra- 
nial pressure, and the special, or focal, due to the particular location 
of the neoplasm and the part of the brain that is damaged. 

The important general symptoms of a tumor of the brain are 
headache, choked disc, retardation of the pulse, vomiting, vertigo and 
generalized spasms. While the objective symptoms are the most re- 
liable for diagnostic purposes, the subjective, especially the headache, 
are usually the first to appear or be noticed. 

Cephalalgia occurs in about two- thirds of the cases and is very 
variable in character. It is less paroxysmal and more progressive than 
most other headaches. It is usually generalized over the whole head, 
though there are at times tender spots, especially upon percussion with 
the fingers. Very often, in spite of its constancy it undergoes sudden 
and sharp exacerbations. As a rule it is dull, boring, aching and dis- 
tressing. Its very constancy is exasperating and wearing. At 
other times it is sharp, lancinating and lightning-like. Pa- 
tients are often driven to contemplate suicide, so agonizing is it. It 
breaks the sleep at night, it unnerves the patient and almost upsets his 



THE NON-NEURONIC DISEASES 915 

mind. It is very often worse at night and occasionally manifes 
certain degree of periodicity in its daily appearances. The location of 
the maximum point of the pain is suggestive oi the location of the 
tumor. Occipital headache with the pain extending somewhat down 
into the neck is suggestive of a growth beneath the tentorium, in the 
posterior fossa or cerebellum. Frontal headaches occur when the 
neoplasm is in the centrum ovale whether anteriorly or posteriori)-. 
Superficial tumors very often lie immediately under the tenderest spot 
in the scalp. The focal pain due to implication of the origin of the 
superior branch of the trigeminus often combines with frontal head- 
ache. Forced expiration, sudden jars, difficult defecation, straining 
of all kind, sneezing and coughing usually increase the headache. An- 
other peculiarity about them is that to all forms of medication that 
overcome other headaches, these are steadily resistant. It 
is not clear entirely what is the immediate cause of these headaches, 
though it is assumed to be a pressure and irritation of the membranes. 
In all forms of tumor this symptom is a prominent one, though it is 
less so perhaps in the gliomatous variety and those that grow more 
slowly. 

The most valuable symptom of brain tumor for surety of diagno- 
sis is undoubtedly the appearance of the eye-ground. Choked disc 
occurs in four-fifths at least of all cases. For obvious reasons it is not 
always the first symptom noticed by the patient. He tampers with 
glasses and opticians for his failing sight for a long time, often before 
his headache, until eyesight and other suspicious signs finally drive him 
to consult a physician. It results from a form of optic neuritis which 
may be bilateral or less frequently unilateral. Most commonly it is bilat 
era! but more pronounced on one side than the other, generally the same 
side as the tumor. It is constantly present in tumors of the corpora 
quadrigemina, and in four-fifths of the cerebellar tumors. It is absent 
in nearly two-thirds of the cases of tumor of the pons, medulla and 
corpus callosum. The size of the tumor seems to have very little direct 
influence upon the presence, severity or course of choked dise. It seems 
to be less frequent, however, in tubercle and most frequent in glio- 
matous and cystic enlargements. Irritation, pressure, engorgement ^i 
the nerve sheath and associated meningitis have all probably something 
to do with the causation of the optic neuritis. Tin course of the in- 
flammation is variable though generally progressive. In the end com- 
plete optic atrophy usually obtains. 

The use of the term choked disc may be misleading, diverting tin- 
mind from the primary inflammatory nature of tin- trouble, but if this 
possibility is guarded against it is still a good one t«. emploj in the de- 
scription' of the appearance <>f the fundus caused b) the neopla 
forms of optic neuritis as distinguished from tin- syphilitic and some 
other forms. Primary optic atrophy never develops as a result of 
brain tumor. The sight is not much impaired if the neuritis is moder 
ate, but curiously enough is often diminished as the inflammation sub 
sides. The secondare atrophy that follows it is always a late sign and 

may be useful in indicating an older age in the tumor when the other 
symptoms have been slight or only of recent on 



9l6 THE NON-NEURONIC DISEASES 

Vomiting is the next important symptom and should probably be 
added to the headache and the optic neuritis as one of the pathogno- 
monic tripod of indications of brain tumor. It occurs in tumor of all 
parts of the brain. It is most frequent, pronounced and obstinate in 
cerebellar and pontile neoplasms. It is an early symptom as a rule 
though it seems to be largely an accompaniment of the headache and 
vertigo. It is a true cerebral phenomenon and hence is peculiarly in- 
dependent of the taking of food or of the condition and contents of 
the stomach. It may come on at any moment and is projectile in char- 
acter. A lad whom I saw with a brain tumor had, before consulting 
any physician, adopted the habit of always carrying a towel with him 
for he had been often embarrassed by vomiting under most unexpected 
circumstances. There is not much nausea with the vomiting and the 
examination of the expelled matter fails to reveal any cause for it. In 
a general way it is more characteristic of rapidly growing tumors. 

In about half of the cases dizziness and persistent vertiginous, in- 
toxication distress are spoken of. In rarer instances there are definite 
attacks of rotatory vertigo. When the tumor is in the cerebellum espe- 
cially, these occur in conjunction with forced movements. Sometimes 
the patient complains of vertigo only upon rising or turning suddenly. 
Vertigo is least frequent in tumors of the cerebral hemispheres, some- 
what more frequent when they are located in the central ganglia and 
most frequent when the tumor is in the cerebellum, cerebellar peduncle, 
pons or corpora quadrigemina. It may be explained partly and in 
some cases by the disturbance of those important avenues of afferent 
impulses, the optic and auditory nerves, but it cannot be entirely so 
accounted for. Under the head of vertigo and Meniere's disease, I 
have discussed this symptom and its mechanism somewhat more in 
detail. 

In nearly all cases, sooner or later, the mind is affected. This is 
.a direct effect of the pressure and irritation and not due merely to the 
prolonged suffering caused by the headache. The latter, of course, 
has a depressing and exhausting effect, too. Stupor and coma are the 
common terminal manifestations, especially just before death. It is 
always a sign of great significance. Early in the disease and when 
the tumor is small it may be absent. In extracerebral tumors it is also 
less frequent. The patient seems to.be profoundly asleep and hard to 
arouse. He is dull, heavy and stupid when he is aroused. He seems 
to drop asleep most easily and on the most extraordinary occasions. 
At table he will drop his knife and fork, stop masticating and fall back 
in his chair. Defecation and urination may occur in the same way. 
Early in the trouble there may be only a slight failure of memory, with 
depression and partial lethargy. In other cases there is exhilaration, 
high emotional excitement, silliness, restlessness, delirium or mania 
with hallucinations and delusions. Asylum cases of insanity show upon 
post mortem quite a number of brain tumors. Sometimes the disease 
evokes only hysterical manifestations in individuals predisposed to this 
psychosis. Large tumors and frontal tumors are supposed especially 
to be characterized by these psychic manifestations. 

General convulsions, which, however, are not epileptic in character 



THE NON-NETJRONIC DISEASES 917 

though they are often associated with unconsciousness, occur among the 
general symptoms of brain tumor. They occur in all stages of the dis- 
ease, closely resemble epilepsy, and in some instances are even pre- 
ceded by prodromata. One-fourth of the cases are subject to these 
attacks. Sometimes they are distinctly apoplectiform. True epileptic 
and Jacksonian manifestations occasionally occur. They may even pre- 
cede all other symptoms by many years. These functional attacks may 
range all the way from petit mal seizures up to those of brief, tetanic 
rigidity. Oppenheim suggests that when epilepsy thus occurs it is not 
so much a direct product of the tumor as an independent disease in a 
brain predisposed to the development of both tumor and epilepsy. 

Retardation of the pulse, to forty or thirty beats per minute, is not 
so very uncommon in intracranial growths. It is the result of the 
general intracranial pressure. It is never an early symptom. In 
tumors near the region of the vagus nucleus the pulse rate tends to 
unwonted rapidity. 

It has been found by Gray, Mills, Lloyd and others that the 
cranial temperature is often somewhat raised. As the normal tempera- 
ture of the scalp is uncertain, the abnormal cannot be employed very 
successfully as a means of distinguishing the presence of a tumor. 

According to Bruns, a typanitic or cracked-pot sound is obtained 
sometimes by percussion of the cranium immediately over the site of 
the tumor. In a limited experience I have not been able to observe 
this symptom. Oppenheim says it occurs under other conditions and 
is always present in sucklings. 

Before the days of cerebral localization it was not possible to 
carry the diagnosis of a tumor of the brain much beyond its mere pres- 
ence. Under such circumstances the above symptoms constituted prac- 
tically the whole of the clinical picture so far as the diagnostician was 
concerned. The order of fheir appearance, the relative frequency of 
sensory, motor and special sense phenomena, their limitations, degree 
of severity and other incidents in regard to them, were matters of in- 
terest, but of little practical value. Since the development of our 
knowledge in regard to the special functions of the various parts of 
the brain all of this has been reversed. It is not enough now to diag 
nose the presence of a tumor; we must attempt a definite localization 
of it within the intracranial mass. This undertaking presupposes a 
thorough knowledge of the anatomy and physiology ^>\ the brain, the 
chapters upon which, as well as the chapter np<»n cerebral localization, 
should be consulted by the reader. I hie. however, a nw words upon 
the focal diagnosis of intracranial growths art- in order to comprehend 
what is said elsewhere and to emphasize tin- clinical picture produced 
en masse by the peculiar localization of- the tumor. 

Whereas the study of tin- general symptoms upon which the diag 
nosis of the mere presence of the tumor is based takes precedence 
always in point of time tin- search for and stud) of the particular 
manifestations upon which tin- definite localization of the growth is 
found far outrank it in importance. \s the signs of localization | 
suppose and include all those that indicate th«- existence of the tumor. 



9l8 THE N0N-NEUR0N1C DISEASES 

they alone would constitute the basis for the diagnosis if they were 
always present. 

Localizing symptoms are not always present. Their absence 
is to be accounted for in three different ways. In some cases the 
morbid growth is so large, and the intracranial pressure is so high 
that the general symptoms overwhelm and completely mask 
all localization signs when they are present. In other cases the neo- 
plasm, small and capable of provoking sharply defined localization 
symptoms, is embedded in one of the so-called silent parts of the brain, 
as, for instance, the frontal and temporal lobes of the right side. 

Multiple tumors may produce such a confused clinical picture that 
the focal signs, though present, are of little use in the diagnosis. Dana 
affirms that one-seventh of all tumors are multiple, including, chiefly, 
tuberculous, cancerous and melanotic growths. And finally in still 
other cases there may be all the while fine and definite localizing mani- 
festations present which our knowledge of brain physiology falls short 
of interpreting. Much as we know of the functions of the brain, there 
is much still, as, for instance, in the production of the mental phe- 
nomena, that we do not yet know. A few gross motor and sensory 
manifestations do not exhaust all of the functional activities of this 
wonderful organ and in our localization researches upon it we have 
only entered the outer portals of its mysteries. Not more than one- 
third of its cortex and its constituent elements are in direct communi- 
cation with the outer parts of the body by way of the nerves, and most 
of our symptomatologies are drawn from the body and neural mani- 
festations. What symptoms, beyond the few mental symptoms now in 
our possession, we are to attribute, directly or remotely, to the mys- 
terious workings of the remaining two-thirds time alone can tell. 

In many cases of brain tumor none but general symptoms occur 
throughout the entire course. In others the localizing signs are dis- 
tinct and definite, even in some instances overshadowing the general 
symptoms. As a general axiom it may be said that the smaller the 
tumor and the less marked the signs of intracranial pressure, the more 
definite and direct will the focal symptoms likely be. A small tumor 
may rarely be located in a functionally known part of the brain and 
yet no localization symptoms be manifested. Such a growth in the 
white substance of the cerebrum has slowly separated the fibres without 
functionally damaging them. Again, what is called action from a dis- 
tance may lead to an erroneous focal diagnosis, but this is exceedingly 
rare. Much more important among these indirect manifestations of the 
tumor are what are called the neighborhood symptoms. If carefully 
studied, these indirect symptoms sometimes add to the value of the 
direct and so confirm the focal diagnosis. 

The best way to discuss the focal symptoms of brain tumor is 
perhaps to take up seriatim the old established anatomical divisions of 
the encephalon, the fossae of the skull and finally some particularly 
prominent centers of the brain. 

Frontal Lobe. — Tumors in the anterior part of the frontal lobe, 
the prefrontal region, do not produce any characteristic motor or sen- 
sory symptoms. There is a change in the character and temperament. 



T H E NO X - N E L' RO N 1 C DIS EA S ES 



910 



generally, of the patient. He is elemented, is dull or extremely emo- 
tional. He laughs and cries easily, is silly and quickly angered. This 
is more apt to be the case when the left lobe is affected ; tumors oi the 
right lobe are as a rule absolutely silent. As the tumor grows and 
compresses and extends backward and downward other symptoms arc- 
added to the mental. Encroachment upon the posterior part of the 
frontal lobe and the central convolutions causes irritative motor signs 
such as muscular spasm. The speech center may be involved in the 
third left frontal convolution causing aphasia, preceded by a sort of 

FIGURE 201. 







(From Sprat ling.) 

distaste for speech, a mutism. Tumors in the inferior part of tin- 
may produce olfactory and visual disturbances b) compi the 
olfactory and optic nerves. In this way hemianopsia and optic neu 
ritis of a severe type ma> be produced. Even the orbit ma) U 
vaded and the ocular globe paralyzed and protruded. When Un- 
conjugate deviation of the eyes with muscular spasm in tin- 
face, the diagnosis of frontal tumor is positive. Brans' invesl 
have revealed to US why frontal tumors sometimes produ< Har 
' 1 1 ' 1 \ 1 a 

Parietal Lobe.— Excluding the posterior central 
mors of the parietal lobe cause preeminentl) senson ma 
They are not prominent and with them are mingled neighborhood 



920 THE NON-NEURONIC DISEASES 

symptoms. The muscular sense is lost, as a rule, and therefore the 
gait is ataxic. As with the frontal lobe, if the growth encroaches upon 
the central convolutions, spasms, contractions, convulsions and paraly- 
ses may occur in the related muscles. The lower limbs are affected 
by high situated tumors, the arms, neck and head by the lower ones. 
As many tracts between the occipital lobe and the central course 
through the white areas of the parietal lobe, tumors in its lower part 
give rise to alexia and visual aphasia. Still deeper growths may cause 
hemianopsia. Near the angular gyrus is the cortical representation 
of the third nerve and its damage has resulted in paralysis of this 
nerve. This may explain some rare cases of vertex gummatous men- 
ingitis with motorocular palsy. I once saw such a case. The symp- 
toms of the specific meningitis pointed clearly to the vertex of the 
brain and the only cranial nerve that was involved was the third. 
Some symptoms of a sensory character due to implication of the 
parietal cortex are probably neighborhood symptoms and due to the 
close connection between the cortical elements of the parietal lobe and 
those of the central convolutions. Astereognosis is a symptom of parie- 
tal tumor in nearly all cases. 

Central Convolutions. — These are the most responsive areas of 
the brain from the standpoint of localization. Being chiefly motor 
in function, and grouping the entire musculature of the body in their 
representation, their injury can be studied objectively and in detail. 
They constitute the motor zone and exhibit most pronounced focal 
manifestations. With the size of the tumor, of course, will vary the 
extent of the manifestations throughout the movements of the body. 
Irritative- signs are among the first to appear and as a result Jack- 
sonian epilepsy obtains. Sensory aurae often precede the local spasms. 
If the tumor is small the epileptic condition may be without disturb- 
ance of consciousness and be confined to the face or the arm or the 
leg. As the neoplasm enlarges, however, the muscular convulsions be- 
come more extensive and the consciousness may be lost, the whole 
clinical picture assuming the complexion of a typical grand mal seiz- 
ure. Even in these elaborate cases, the consciousness is not lost at first 
and the aurae and spasm usually begin always in the one place, thus 
enabling the localization to be made. The hemiplegic character of the 
primary manifestations should be carefully noted. As the destructive 
action of the tumor goes on, the spasms are replaced by a gradually 
deepening paralysis. Monoplegias and hemiplegias are the forms that 
this assumes. Sensory disturbances usually accompany them, con- 
sisting of various paraesthesiae such as numbness, pricking, pins-and- 
needles sensation, loss of pain, touch and temperature sense, and even 
complete hemianesthesia. Even the muscular sense may be involved 
and the stereognostic sense. Local twitchings in certain muscular 
groups, followed by spasm and paralysis in the same groups, asso- 
ciated with similar sensory phenomena in approximately the same 
localities, are the sign manual of a growing neoplasm in the central 
lobule. Aphasia and agraphia may also be present. The exact point 
of the cortex impinged on and the details of the localization can be 
worked out by reference to the chapter on cerebral localization. It 



THE NON-NEUHONIC DISEASES 0,21 

must be remembered that the tumor may not actually be in the cen- 
tral cortex. It may be in the meninges over the center or in the white 
substance of the brain beneath it. Under such circumstances irritative 
symptoms of the motor centers will be very gradual in onset, paroxys- 
mal in character in the beginning and only very late become posi- 
tively and permanently paralytic in character. However, there is great 
uncertainty about this as well as about the age and size of the tumor 
from such localizing indications. A very large tumor, for instance, 
of the centrum ovale may just touch the motor centers, as it were, 
and produce only slight irritative symptoms. 

It is thus obvious that implication of the motor zone of the cor- 
tex furnishes us with our happiest localizing symptoms. Their origin, 
their location and their onward march from slight twitching to com- 
plete paralysis are seen in no form of lesion so beautifully and regu- 
larly characteristic as in tumor in or about this region. 

Temporal Lobe. — In right-handed people the right temporo- 
sphenoidal cortex is practically latent. In the left temporal cortex 
are the centers for hearing and smell and taste. Word-deafness occurs 
with tumor of the first and second convolutions, also amnesic aphasia 
and various forms of paraphasia. Pressure by a temporal tumor on the 
neighboring parts of the brain may cause a variety of symptoms. 
Posteriorly it may provoke optic aphasia : anteriorly it may disturb 
the centers for taste and smell both in itself as well as in the cornu 
ammonis. If the tumor is verv low in the lobe so as to compress the 
medulla and adjoining parts it may cause attacks of vertigo with forced 
movements and a mixed type of aphasia. Hemianesthesia, hemiplegia 
and hemianopsia may all be caused by such a localization of the neo- 
plasm. The reason is clearly the implication of the great conducting 
tracts in the brain stem. 

Occipital Lobes.— The" visual centers of the cortex are the great 
characteristics of these lobes. A bilateral tumor in them produces 
complete amaurosis. Hemianopsia is the distinguishing feature i>\ a 
tumor in one of the lobes. As lesions of the optic tract may cause 
the same visual disturbance, it is not a particularly valuable sign for 
locating the tumor in the occipital lobe. When, however, it is accom- 
panied by sharp occipital headache, extending down the neck the pre- 
sumption is strong that the growth is occipital. Psychic blindness, 
word-blindness, soul-blindness or the incapacity t«» comprehend the 
nature of things seen are some of the curious results of tumors in the 
occipital lobe. 'Extension of such a tumor int.. the parietal lobe and 
impingement upon the internal capsule may be surmised by the hemi- 
anaesthesia, unilateral ataxia, and even hemiplegia. 

Central Ganglia.— -Tumors of this region like those «-t tin- corpus 
callosum are only obscurely diagnosed and from the standpoint 
surgical intervention are of no interest whatever. Most of the symp- 
toms are due to the damage done to the internal capsule, either 
directlv or through pressure. Gradual and partial hemiplegi 
distinctive symptom <>r there may be unilateral, indefinite twitchi 
from a tumor in the striate- body <>r the thalamus irritating the 1 
SUle and its fibres that go coursing down between them. Hemichoi 



922 THE NON-NEURON IC DISEASES 

athetoid movements on one side of the body, involuntary and automatic 
jactitations, hemiansesthesia and hemianopsia of the opposite side, are 
all possible and their mechanism easily understood. There are no 
known symptoms produced by a growth confined solely to the cor- 
pora striata or optic thalami, unless it be located in the posterior 
part of the latter or pulvinar. Growths in the pulvinar cause hemian- 
opsia with distinctive hemiopic pupillary reaction or inactivity, a fact 
which distinguishes this form of hemianopsia from that produced by 
disease in the occipital lobe. Tumor of the basal ganglia is usually 
marked by a considerable degree of stupidity. 

Corpus Callosum. — Tumors here are not frequent and their focal 
symptoms are not very distinctive. There is a peculiar mental state 
consisting of intense stupidity, drowsiness, sopor, mutism and mental 
deadness. For hours the patient will sit immobile, seemingly lost to 
every stimulation from the outer world. The absence of most of the 
localizing signs of tumor and the gradual increase of those that are 
present are two of the more striking features of tumor in this re- 
gion. Absence of cranial nerve disturbances and absence of anaes- 
thesia are especially noteworthy. Hemiplegia with a lesser degree of 
paralysis on the other side, or bilateral hemiplegia of equal intensity 
on both sides, is suggestive. Coma usually terminates these cases. 
Dana thinks that symptomatically tumors of the great commissure are 
the same as or closely correspond with tumors situated in the third 
and lateral ventricles. In other words they belong to all of that class 
of tumors which begin in the central parts of the brain and gradually 
extend outwards toward the periphery. 

Corpora Qnadrigemina. — Tumors here usually involve also the 
crura cerebri and pineal gland, or vice versa. These structures are 
very complex and important organs. In them are located the pri- 
mary centers of sight and hearing. Their occupation by a tumor 
therefore causes hemianopsia or blindness, impaired hearing or deaf- 
ness. With this hemianopsia there is paralysis of the ocular muscles 
as a rule. The pupillary reflex is lost and there is nystagmus. Ambly- 
opia may occur and the same ocular muscles may be paralyzed bilat- 
erally. Incoordination, forced movements and an intention tremor, 
as well as a tremor like that of paralysis agitans, may often be ob- 
served. Most of these are neighborhood symptoms and occur whether 
the tumor have its origin in the pineal gland, the gemina or the crura. 
A special characteristic of implication of the latter is superior alter- 
nating hemiplegia, a condition in which there is oculomotor paralysis 
of one side with paralysis in the extremities of the other side. A 
curious and rare analogue of this is the alternation of oculomotor 
palsy with a hemiataxia of the other side, due, according to KrafTt- 
Ebing, to a tumor in the tegmentum. These latter conditions are ex- 
tremely rare. 

Cerebellum. — Cerebellar tumor of a certain type is perhaps the 
most definite of the localizable lesions. Its diagnosis is therefore com- 
paratively easy. Tumors in the lateral lobes of the little brain are 
usually silent until they press upon the medulla, the pons and the re- 
lated cranial nerves, when they produce close neighborhood symptoms. 



THE NON-NEURONIC DISEASES 923 

Vertigo and incoordination are the distinctive symptoms, though not 
strictly focal, of a neoplasm in the middle iobe or vermis. Cerebellar 
ataxia is a reeling, drunken gait. It has been called a titubating 
gait It is unfortunate that the term unstable equilibrium is not used 
instead of ataxia, because the gait is not the same as that seen in tabes. 
A true ataxia may develop rarely in the extremities and be bilateral 
or unilateral. Sometimes closing of the eyes increases the disturb- 
ance of equilibrium and on account of it the patient may actually fall. 
A distressing and constant vertigo accompanies usually this symp- 
tom. Vomiting, appearing early and continuing during the entire 
disease, is a typical symptom. Forced movements, turning involun- 
tarily and automatically one way or the other, are also quite prominent 
in some cases. The general symptoms of this tumor are st rough 
marked, as a rule. The headache is occipital and extends with mus- 
cular rigidity into the neck. It may be frontal in some cases. ( )ptic 
neuritis is sharp and well defined. Opisthotonos, general convulsions. 
tetanic rigidity of the whole body, unilateral and bilateral hemiple- 
gia, may all occur from extreme pressure upon the great tracts run 
ning through the medulla. Other medullary symptoms that may not 
be unlooked for are glycosuria, cranial nerve and nuclei disturbance 
and the usual signs of bulbar paralysis. Internal hydrocephalus is 
also possible from pressure on the venae Galeni. 

Pons Varolii and Medulla Oblongata. — These parts of the brain 
are subject more frequently to tuberculous and gliomatous tumors 
than to any other variety. Occasionally no symptoms are produced 
by them for a long time but sooner or later a very characteristic clin- 
ical picture is presented. The details of this picture ma\ 
undergo a great variety of presentations but in the main 
its chief outline is quite uniform. The prominent feature in the 
symptomatology of tumors^ of the brain stem is the combination of 
cranial nerve palsies and hemiplegia. In most tumors the cranial 
nerve palsy will be on the same side as the tumor, the paralysis of the 
limbs on the opposite side. This is the well-known alternating hemi- 
plegia and is easily comprehended by a glance at the physiological 
anatomy of the parts. The paralysis of the limbs will, ^i course, be 
of the cerebral or central neurone type, while that of the cranial 
nerves will be of the spinal or peripheral neurone type. The size and 
exact location of the tumor must l>e worked out 1>\ a stud) of tin- 
particular cranial nerves involved and the extent of the henupKy 
In about one-quarter of the cases the cerebral nerves alone are in 
volved, in another quarter the limbs are affected, in nearh a half 
are both the nerves and limbs involved. In almost eight \ five per 
cent, of the latter the paralysis i^ of the alternating variety. In high 
tumors of the pons the hemiplegia is combined with oculomotor paralj 
sis; in low tumors with trigeminal paralysis. Lower down still in 
the medulla the other nerves ma\ hi- Involved seriatim such as the 
facial, the abducens, the auditory, etc. Bilateral cranial nerve palsy, 
bilateral hemiplegia and all the symptoms of a true progressive bulbar 
paralysis may appear when the tumor is large, bilateral ..r t <nt rails 
located. If it is situated vm laterall) forced movements ma) be a 



924 



THE N0N-NEUR0N1C DISEASES 



FIGURE 202. 




Nerv 



Schematic representation of the course of the pyramidal tract for the face and 
for the extremities. A lesion above the facial decussation causes paralysis of face 
and extremities on the side opposite the lesion ; a lesion below the facial decussa- 
tion causes paralysis of the face on the same side and of the extremities on the 
side opposite the lesion. The latter condition is known as "crossed paralysis' 
or alternate hemiplegia. (Diagram modified from Edinger.) 



THE NON-NEURONIC DISEASES 925 

feature of the case with general unilateral or alternating convulsive 
movements. In pontile tumors sensory symptoms with hemiataxia 
may also occur. Most unexpected and extraordinary combinations 
are liable to occur. The conjugate deviation of the eyes, sometimes 
accompanied by facial palsy, is toward the side opposite that of the 
lesion, and thus is different from the conjugate deviation from a cere- 
bral lesion, in which case it is toward the side of the lesion. Disarthria 
and dysphagia may occur with pontile tumors. 

When the growth is below the pons in the medulla bulbar symp- 
toms stand prominently forth. Hemiplegia, hemianesthesia with 
paralysis of the ninth, tenth, eleventh and twelfth nerves constitute 
the essential elements in the clinical presentation. All those symp- 
toms usually associated with implication of the floor of the fourth 
ventricle may be expected such as dysphagia, dysarthria, aphonia. 
<leafness, etc. Irregular heart action, respiratory embarrassment, vom- 
iting, retraction of the head and neck, glycosuria, vasomotor phenom- 
ena are among the usual signs of tumors in this part of the encephalon. 
The gait may be unsteady as in so-called cerebellar ataxia, or the limbs 
may be unilaterally or bilaterally paralyzed both in motion and sensa- 
tion. General intracranial pressure may or may not be developed. 
Convulsions usually close the scene in most cases. 

Tumors of the base of the brain are conveniently localized into 
those of the anterior, middle and posterior fossae of the skull. The 
main symptoms of such tumors have been referred to when the cor 
responding lobes of the brain were discussed. There are a few pecu- 
liarities about basal tumors that deserve further mention, however. 
They may break through into the cavities of the forward part <n the 
skull. The nose, the pharynx, the antrum, the tympanum have all 
thus been entered and the functions of the corresponding and ad- 
joining organs damaged. In such instances palpation, as through the 
mouth, reveals an unusuaf sensitiveness of the brain in that situation. 
Debris, hemorrhage and pieces of the broken down tumor may be 
thus extruded and the nature of the growth be accurately diagnosed. 
Optic neuritis, optic atrophy, less frequently than in other tumors, 
choked disc, cranial nerve implication are all to be observed in cases 
of basal tumor. If the growth is extradural, there may be no local 
Izing signs until late. 

Anterior Fossa. — In addition to what has already been said about 
intrusion of the orbital, nasal, pharyngeal and maxillary cavities b) 
tumors growing in the anterior Fossa, symptoms occur that are tin- 
same as those when the growth is in the frontal lobes. Especially 
characteristic are the mental and temperamental changes. ( Ufactory, 
optic and oculomotor disturbances are particularly suggestive Pal 
mia may be present for a brief period but anosmia occurs sooner "t 
later from destruction of tin- olfactory lobes. Loss of smell, it must 
be rememben-d. has occurred from tumors elsewhere in ran 
due. according to an unproved hypothesis, t<. a neuritis of tin- olfac 
tory such as occurs in tin- optic nerves. The -aim- ma) be said, 
ceptino- the hypothetical nature of tin- nerve lesion, of tin- optic neu 
ritis that is seen in tumor- of tin- anterior fossa. Ks these neopla 



926 THE NON-NEURONIC DISEASES 

rarely remain confined to the anterior part of the skull, symptoms may 
occur in them showing implication of the optic chiasm and even of the 
crura. 

Middle Fossa. — These tumors may cause erosion into the tym- 
panum with complete loss of hearing, or the deafness may be due 
to the extension of the tumor and implication of the auditory nerve. 
The fifth nerve and the Gasserian ganglion are particularly exposed 
to the damaging influence of these tumors. Neuroparalytic ophthal- 
mia is a very characteristic symptom. With the extension of the 
tumor the facial is usually involved with the auditory nerve. Symp- 
toms of optic nerve and chiasma involvement are particularly char- 
acteristic. The hypophysis is often the seat of tumors that cause 
these visual disturbances. The condition is observed in acromegaly 
and will be again referred to in the discussion of that disease. Bitem- 
poral hemianopsia, unilateral and bilateral amblyopia, unilateral 
amaurosis with hemianopsia in the other eye. complete blindness and 
other pronounced phenomena may occur. The case whose chart is 
shown in the chapter on acromegaly had at one time blindness of the 
two lower half-fields, horizontal hemianopsia. This was so curious 
that hysteria was one of the early diagnoses made in the case. It 
proved to be sarcoma of the hypophysis with complete atrophy later on 
of the optic nerves. 

For a while sometimes the fundi of these cases show no changes. 
Signs of injury to the optic chiasm are almost pathognomonic of tu- 
mors of the middle fossa. The third nerve, however, is frequently 
included though less so than the optic. Exophthalmos with contrac- 
tion of the pupil may be the only signs in the beginning that can be 
detected objectively. Reflex twitchings in the facial may be another 
early sign. Extension of these middle tumors forward may provoke 
slight mental exhibitions or, if they reach backward, crural symp- 
toms such as hemiplegia, hemianesthesia and rarely convulsions may 
be observed. 

Posterior Fossa. — With neoplasms in the posterior fossa, cere- 
bellar, pontile, medullary and cranial symptoms occur in a great 
variety of combinations. They may be unilateral or bilateral. As 
the growth begins outside of the brain stem and extends inward, the 
cranial nerves are apt to be affected before the hemiplegia appears, 
which is the reverse or at least different from what obtains in internal 
tumors. It is obvious also why in such tumors facial and auditory 
nerves are implicated together, and internal strabismus occurs in one 
eye with the conjugate deviation of the other, as will occur if the 
sixth nucleus is the primary seat of the trouble. A general com- 
pressive bulbar paralysis is the typical picture produced by these pos- 
terior cranial growths. 

Speech may be affected in several ways by intracranial neoplasms 
according to their location. When the site is the third left 
frontal convolution or the immediate vicinity, motor aphasia is the 
character of the disturbance. Amnesic aphasia and paraphasia occur 
from tumors in the first left temporal convolution and its vicinity. 



THE NON-NEURONIC DISEASES 927 

Dysarthria, anarthria and aphonia may result from tumors in the 
middle oblongata or in the posterior fossa of the skull. 

Visual disturbances are varied and numerous from intracranial 
neoplasms. The visual impulse after it leaves the retina traverses 
a long tract and through many parts of the brain before it finally 
reaches the occipital cortex. Hemianopsia must always be studied 
in conjunction with the other symptoms if it is to be employed in 
making a focal diagnosis. It may be the result of a lesion anywhere 
in the tract behind the optic chiasm. If the tumor is in the optic tract 
proper, other cranial nerves, especially the oculomotorius. are apt to 
be included. If the thalamus is the site of the trouble, the conduct- 
ing paths in the capsule are involved and hemianaesthesia and hemi- 
plegia are associated with the hemianopsia. When the growth nests 
in the corpora quadrigemina, external and internal ocular paralysis 
occurs. Aphasia with hemianopsia indicates implication of the optic 
tract as it courses backward to the left occipital lobe. A tumor oi 
the occipital lobe itself produces hemianopsia as the only visual symp- 
tom. If the tumor is bilateral 01 so large as to injure the cuneus in 
both occipital lobes amaurosis obtains. Mind-blindness occurs with 
occipital tumors. 

The sphincters of the bladder and bowel are not affected by brain 
tumor though evacuation may seem to take place involun- 
tarily in the state of stupidity and mental apathy that more 
or less accompanies all intracranial neoplasms. The polyuria, 
glycosuria and albuminuria that may occur in tumors of the 
brain stem have been mentioned. As they may be due to the general 
intracranial disturbance they are only of limited value as localizing 
symptoms. 

Diagnosis. — The diagnosis of a tumor of the brain is never a 
simple matter, though it is easier in some cases than in others. It 
should always be made upon the complexus of symptoms in tot >, 
rather than upon any one or two of them. As many signs should be 
discovered therefore as possible. Some cases arc- latent and present 
no signs at all, for a long time at least. Others exhibit only on, 
two symptoms, like headache, for instance, long, even years, before 
the appearance of others. Some cases present only the general symp- 
toms ; now and then a rare rase may exhibit merely some one or two 
focal, without general, manifestations. M<>m cases present both gen- 
eral and focal symptoms sometime in their course though the loca 
tion of the tumor, its age. its nature and man) Other factors will v;ir\ 
very greatlv the relative values of tin- respective general and focal 
symptoms. Subjective symptoms are commonly tin- first t<> be no 
ticed; objective symptoms are tin- most reliable for diagnostic pur- 
poses. Though the patient usually presents himself on account 
the headache, the examiner should at once institute a minute search 
for objective signs. The most important of the latter is without doubt 
optic neuritis. No headache should be allowed t<> pass without a careful 
examination of the eye-grounds. From eighty t<> ninet) per cent, of 
the cases of intracranial tumor have optic neuritis and choked disc. 
It is a characteristic condition and is not exactl) like other fomu 



9^8 THE N0N-NEUR0N1C DISEASES 

optic neuritis. It is practically confirmatory of the trouble. A some- 
what similar choked disc occasionally appears in meningitis, cerebral 
abscess, renal disease and hydrocephalus, but these can be distin- 
guished by other symptoms. Papillitis may be due to other causes 
than tumor, especially when chlorosis, lead poisoning, polyneuritis 
or alcoholism are present. A central scotoma for colors speaks for 
alcoholic intoxication. With the headache cerebral vomiting is almost 
always present. Vertigo is also a frequent accompaniment. 

The headache must be studied from every possible point of view. 
It is usually characteristic in brain tumor though often it varies from 
the typical and by resembling other forms of headache, like hemi- 
crania, the cephalalgia of hysteria, neurasthenia, constipation, infec- 
tion and toxaemia, may add much confusion to the diagnosis. It is well 
in such cases to diagnose the neoplastic headache by exclusion. A 
search should be made for all possible causes of the headache apart 
from tumor. If then papillitis and vomiting can be added to the symp- 
tomatology the diagnosis is complete. Cephalalgia, optic neuritis, 
cerebral vomiting, constitute strong grounds for the opinion that a 
tumor is present. As these symptoms are not always present all to- 
gether there are others that when added to any one of these makes 
the diagnosis strongly presumptive, practically positive in some cases. 
Vertigo is not of much importance. Progressive stupor is, however ; 
so also are retardation of the pulse, general convulsions, epileptic 
attacks of a particular type and various speech disturbances. The 
progressive character of the symptomatology is a significant feature. It 
will be noticed that all of these symptoms except the optic neuritis 
may occur in certain non-organic diseases, such as hysteria, neuras- 
thenia, epilepsy and certain psychoses. It is necessary to exclude 
these first, therefore, which may be generally readily done by search- 
ing for the other symptoms of these various neuroses. It is to be 
remembered, however, that as a rare possibility a latent tumor may 
be present with all the signs of a mere neurosis or psychosis. Of 
course, no differentiation can be made then. 

An organic disease, and that a tumor of some sort, being finally 
decided, the location of it is the next question to be considered. I 
have shown under the head of symptoms how the focal diagnosis may 
be both clear and obscure. I have also dwelt upon its supreme im- 
portance. While so strongly suggestive of a neoplasm, focal symp- 
toms are sometimes produced by other diseased conditions, as for 
instance, a focal meningitis, an aneurism, an old hemorrhagic cyst 
or spot of necrobiosis. Even in hysteria, epilepsy, alcoholism, uraemia 
and paralytic dementia localized manifestations both of a motor and 
sensory character in various parts of the body may occur in such a 
way as to closely simulate the focal symptomatology of brain tumor. 
The progressive character of the latter taken in conjunction with 
the characteristic general symptoms helps much in the differential 
diagnosis. It seems incredible how closely even focal organic symp- 
toms may be simulated by the neuroses and diffuse organic diseases. 
Gowers mentions the case of a hysterical little girl who after watch- 
ing for some time a genuine case of brain tumor, mimicked it almost 



THE XOX-XEUROXIC DISEASES 



929 



perfectly. Monoplegias, focal anaesthesia, limited irritative and de- 
structive simulacra and actualities may occur under many other cir- 
cumstances, functional as well as organic, than those of an intracra- 
nial growth. The keeping close to the typical symptomatology of 
tumor and contrasting it with the total symptomatology or entire clin- 
ical picture of these other diseases is the only safe way to determine 
the origin and focal value of the former. 

The presence of a tumor and its location having been established, 
it remains only to fix its nature. As multiple tumors are always in- 
operable, whatever their location may be, they must be carefully dis- 
tinguished from single growths. Such tumors do not, as a rule, 
afford any definite localizing symptoms by which an operation can be 
guided anyway and so the diagnosis of the single tumor is the great 
desideratum after all. It is not always easy by any means to deter- 
mine what sort of a growth the patient is afflicted with. Certain gen- 
eral infectious states, such as syphilis and tuberculosis, will afford a 
strong presumption as to the nature of the neoplasm. The existence 
of tumors in other parts of the body, like cancer of the breast, actino- 
mycosis of the jaw, hydatids of the liver, presupposes the same sort 
of a tumor in the brain. Tubercle and gliomata occur most frequently 
in the cerebellum and brain stem ; sarcomata at the base of the brain 
and outside of it; syphilomata in the cortex. The rapidity of growth, 
general course and extension of the tumor help slightly to suggest its 
nature. Cerebral gliomata are slow and gradual in their development 
Tumors that are rapid at first and then stationary are probably tuber- 
culous. The results of treatment will occasionally determine a syph- 
ilitic neoplasm from all other varieties. 

The main diseases from which intracranial tumor is to be care- 
fully differentiated are epilepsy, migraine, hysteria, alcoholism, lead 
intoxication, abscess, intracranial aneurism, dementia paralytica, acute 
encephalitis, disseminated cerebrospinal sclerosis and melancholia. The 
reader is referred to the sections upon these various affections for 
their differentiation from tumor. 

Lumbar puncture has been found useful in the diagnosis of a few 
obscure cases. Increased pressure, leucocytosis and the presence of 
bacteria may point to a tumor and meningitis, though their absence 
does not exclude the former. 

Lately skiagraphy has been employed to locate a cerebral tumor. 
In some instances, particularly when the growth was superficial or 
near the vertex, the shadow w. tiring. In deep tumors the 

Rontgen ray does not seem to be of much availability. Metal obj< 
such as shot and bullets are much more distinctly seen in skiagraphs 
than are the ordinary tumors. 

Prognosis. — The course of brain tumor is usuall) a prolonged 
one, ranging from a few months to - t number of years. Jackson 
ported a glioma that had apparently lasted for ten years, and I >sler 
one in which Jacksonian symptoms had persisted for fourteen y< 

Most of the cases run their career in about two or three 

duration of the tumor (Upends upon its nature somewhat and the ter 

mination of the case is often effected by the destruction of the neigh- 



93° THE NON-NEURONIC DISEASES 

boring brain substance. Gliomata and fibromata are the most en- 
during tumors. Especially prolonged are cholesteotoma and angioma. 
Carcinoma, some varieties of glioma and soft sarcoma are apt to be 
rapid. Tubercle, especially when it appears in childhood, and even 
other forms of tumor, have become stationary. Syphiloma is the only 
tumor that seems capable of disappearing entirely, and then only un- 
der treatment. It, as well as partly degenerated gliomata, may leave 
permanent residua. By discharging their degenerative debris through 
the nose and mouth, the effects of certain growths have been quite 
ameliorated. Very rarely a brain tumor may become encapsulated 
or atrophied, with a recession of its symptoms. In other cases after 
a long period of quiescence" or slow progress it may suddenly light 
up most violent symptoms with coma and the patient pass quickly to 
his death. Altogether tubercle in children and gummata in adults 
offer the most favorable .prognosis : rapidly progressing gliomata and 
sarcomata the most. A sarcoma may prove fatal in six months. Lo- 
cation of the tumor has much to do with the prospect of the patient's 
continued existence. Bulbar tumors are particularly dangerous. 
Subsidence of the headache, and recession of the optic neuritis, are 
favorable signs of a possible recession or stationary condition in the 
neoplasm, or at least its environment. Marked mental stupor, con- 
vulsions, severe vomiting, rapid and intense optic neuritis and apoplec- 
tic seizures are bad omens. I have seen a marked recession of all 
symptoms with an ultimate optic atrophy remaining in a case which 
several years ago had been told by several competent neurologists that 
he could not possibly live the year out. 

Our prognosis should always be made guardedly in cases of brain 
tumor. A slow, chronic optic neuritis indicates that the disease will 
probably be of slow progression. 

Spontaneous recovery has been seen in the parasitic tumors, and 
spontaneous metamorphosis and retrogression are believed by some 
to occur sometimes in tubercle. 

It is believed that some reported cases of the disappearance of 
all symptoms of brain tumor were cases of Quincke's serous menin- 
gitis or idiopathic internal hydrocephalus. 

Death results from bulbar symptoms, exhaustion, infection, com- 
plications and intercurrent maladies. 

Treatment. — Every case of tumor presents a study for medical 
and surgical treatment. In this is included the question of radical 
cure or only amelioration. In most cases the entire treatment of the 
case resolves itself into the management of the patient and his comfort, 
without any hope or attempt at modifying in the least the morbid 
growth. 

The administration of medicines will have, therefore, for its 
twofold object the eradication of the tumor and the relief of the pa- 
tient's sufferings. A clear comprehension of the limitations of the 
medical treatment of brain tumor will not only lead to the avoidance 
of some ridiculous errors and absurd logic but it will enhance the 
value and efficacy of the small powers with the limitations. A mere 
temporary relief of the headache will not be interpreted then as a 



THE NON-NEURONIC DISEASES 93I 

cure, a diminution of the convulsions will not be looked upon as a 
hopeful sign of the disappearance of the neoplasm, nor will the diag- 
nosis previously well founded be shaken by mere temporary changes 
in the general clinical picture. On the other hand, what can be done 
by medicinal agents in a few cases will be so sharply defined that there 
will be no hesitancy or lack of energy in applying the few effective 
measures in the properly selected cases. Therapeutic sins of omis- 
sion as well as commission are sometimes strikingly enacted in eases 
of brain tumor. In no disease is prompt, thorough, correct treatment 
so much of a desideratum, and in no disease are the indications for 
it more obscure sometimes. Time must not be wasted with medicines 
if the tumor falls into the operable class soon to be mentioned. Sur- 
gery must not be coquetted with if the tumor is amenable to medical 
treatment or is inoperable. Symptomatic relief, by all available and 
surgical means, must be promptly and fulsomely given if all hope of 
affecting the tumor itself is past. In a word, given a correct diagno- 
sis of the location and nature of the growth, and a thorough appre- 
ciation of its proper relationship to medical and surgical interven- 
tion, the treatment should be prompt, thorough, rational and perma- 
nent. 

The treatment of syphilomata by appropriate medication is not 
only successful but it furnishes us sometimes with some of the most 
brilliant results known to medical science. The disappearance of some 
of the most threatening symptoms is accomplished almost as if by 
magic. The more recent the tumor and the shorter the time that the 
focal symptoms have existed, the more complete and satisfactory is 
the cure. After a syphilitic growth has existed for a long time and 
irreparable changes have taken place in the brain tissue, no treatment 
can be expected to banish the manifestations that depend upon those 
changes. And yet even irr many advanced and old cases of this sort. 
a decided and grateful retrogression of the symptoms is often brought 
about by antisyphilitic treatment. Every case that presents a history 
or suspicion of syphilis should be- at once put upon antispecific reme- 
dies. The iodide of potash, started at twenty grains three times a day, 
should be rapidly increased until two or three hundred grains ;i da\ 
are administered. If in a week or two this is not accompanied b\ s< 
change for the better in the symptoms, mercurial inunctions should 
be added to the regimen. For details of the treatment, consult the 
chapter on cerebral syphilis. In tin- case of tumor there is not any 
ground for fear in the use ot this heroic antisyphilitic medication ;i< 
there may be in the degenerative conditions of the parasyphilitic dlS 
eases, locomotor ataxia and paretic dementia. Within reasonable lim- 
its, such as would undoubtedl) show some result, in a genuine case of 
syphiloma, it can do no possible harm whatever the tumor max 

Nay, more, it is a fact that even in non-Syphilitic neoplasms the io,li,le 

of potash has very often caused .1 noticeable amelioration of the head 
ache and other symptoms. Henc< it is good pi i for .1 

short time with antisyphilitic medication all 1 tumor in which 

there is a shadow of a doubt about its specific origin, and in which 
the evidences do not point most emphatically awnv from syphiloma. 



932 THE NON-NEURONIC DISEASES 

By such a procedure under these circumstances there is everything to 
gain and nothing to lose. 

It is extremely doubtful whether any other than syphilitic tumors 
can be directly affected by internal medication. Cases of improve- 
ment and even cure have been reported in tubercle by the use of cod 
liver oil, tonics, rest and a general hygienic mode of life. Gowers says 
that more than once he has known the symptoms of cerebral tubercle, 
steadily increasing under country air and abundant food, to become 
permanently arrested when the patient was taken into a London hos- 
pital and cod liver oil and iron given. It is known, however, that this 
class of morbid growths very often, after a period of rapid and rather 
violent activity, become stationary, and especially so when the gen- 
eral constitution is put in the best condition of health. These happy 
results are most attainable in children, in whom it is believed that 
tubercle has been made to disappear completely. Little as we know 
about the reparative processes of the treatment in these cases, the 
latter is apparently so fortunate in some few instances, that it recom- 
mends itself for all cases of tubercle. The general hygienic and tonic 
treatment can only be of advantage to all cases of tumor, tuberculous 
or otherwise. It is to be hoped that some specific remedy will be dis- 
covered some day to act upon these tubercles as the iodides act upon 
syphilomata. The tuberculins that have lately been experimented 
with in tuberculosis of the lungs and joints, have not succeeded in 
giving any very promising results in cerebral tuberculosis. 

Arsenic has been recommended and said to have shown a cura- 
tive power in a few cases of sarcoma. It is a tonic, as we all know, 
and affects powerfully the metabolism of the body. If it only strength- 
ens the organism so as to give it a fighting capacity against these 
growths, or if it assists in their transformation into more stationary 
forms such as fibrosarcoma, it is a most available agent and should 
be given a fair trial. The same statements apply to phosphorus. 

No other tumors than those just mentioned respond to medical 
treatment and so far as we know no other remedy has any direct 
effect whatever on intracranial neoplasms. Symptomatic treatment 
therefore constitutes the only field for the further use of internal 
medication. This, however, is of great importance and may be called 
for whether an operation be a part of the question or not. The head- 
ache is the chief symptom that calls for relief. Most of the remedies 
that are useful in other forms of cephalalgia are distinguished, as a 
rule, for their incfficacy in this form. Hence in most cases nothing 
but morphine will avail. To be sure there is always the danger of 
the formation of the morphine habit to be taken into serious consider- 
ation. If the nature and location of the tumors are not clear and if 
there is a probability that it may prove to be operable when it an- 
nounces itself a little more definitely, morphine had better be with- 
held and temporizing undertaken with other drugs. Unless the head- 
ache is excruciating, threatening to drive the patient to suicide, as it 
almost does sometimes, all other possible means of relief had better 
be tried first before morphine is resorted to. I prefer to try the fol- 
lowing remedies in the order mentioned: cannabis indica, phenacetin. 



THE NON-NEURONIC DISEASES 933 

acetanelid, antipyrin and large doses of sodium salicylate. Other 
measures commonly employed in the management of headache should 
not be neglected. An ice bag, cold water coil or hot cloths may be 
applied to the head. A mustard foot bath and a sinapism to the back 
of the neck may help somewhat. Purgation, free diuresis and diaphor- 
esis, even leeches and venesection may be considered. As a rule the 
case will prove to be desperate and resort will have to be had to mor- 
phine. In inoperable, severe or moderately severe cases with an un- 
favorable prognosis constantly hanging over them, it seems to me 
more beneficent to establish, if need be, the morphine habit and give 
the patient some comfort the few months or years he has to live, than 
to allow- him to be harassed and worn out, perhaps sooner than he 
would be even with the morphine habit, by the increasing and intol- 
erable headache, vertigo, vomiting and convulsive seizures. For these 
latter symptoms there is sometimes mitigation in full doses of the bro- 
mides, chloral and other narcotic antispasmodics. 

In nearly all cases the question of surgical intervention will arise. 
In not more than five per cent, of the cases will the tumor be found 
to be operable. The early enthusiam following the work of Hors- 
ley, Macewen, Godlee and others has calmed down considerably , but 
yet when we consider what is being done at the present day by such 
operators as Wernicke, Horsley, Bergmann, Keen and others, and 
compare the promising outlook offered by their results with the utter 
hopelessness with which these cases were regarded only a few decades 
ago, we may congratulate ourselves without undue elation upon the 
splendid advances of surgery. 

Five per cent, is not a large number of cases amenable to oper- 
ation but that is not the fault of surgery, it is in a large measure the 
result of the location and nature of these tumors. Multiple tumors are 
inoperable; so also are malignant and metastatic growths. Deep 
neoplasms usually cannot be reached without almost certain risk, hence 
they cannot be undertaken. Large infiltrating growths must also he 
left alone. The infiltration of a small, superficial tumor is not a ground 
for its being regarded as inoperable. The most favorable tumors are 
those that are single, superficial, not too large, more or less encap 
lated and distinctly localizable. These are tin- fibromata, growing from 
the dura and compressing the brain in and about the motor rone. 
Small tumors, early diagnosed, offer the best chances also, though 
large growths have been removed piecemeal in successive operations. 
In some cases in which the localization of tin- tumor is somewhat in 
doubt an exploratory operation is to be recommended. Tumora 
the occipital lobe, causing hemianopsia, and those in the temporal 
lobe which cause auditory disturbances max hi- regarded as amenable 

to the knife. As the opening of the cranial cavity is always a serious 

procedure, the relatives should always Ik informed of all p<>s M bie 
accidents. They should also be made well acquainted with the 
queke that are likely to follow the removal of the tumor or excision 
of the brain substance- with its removal. The continuance of the 

paralvsis should be carefully explained beforehand to them, if the 



934 THE NON-NEURONIC DISEASES 

operator wishes to avoid most awkward questions after the recovery 
of the patient from the operation. 

In some cases, focal symptoms alone may justify an operation. 
A persistent aphasia, especially if it be progressive, may well suggest 
a trepanation over the third left frontal convolution. 

Cerebellar tumors do not encourage one very much to operate. 
Their removal may be possible in adults but is not to be thought of in 
children. The trouble is that if the tumor is in the lateral lobe it does 
not usually produce symptoms until it is too large for surgical in- 
tervention, and if it is in the middle lobe where it usually causes the 
liveliest symptoms, it is in too close proximity to vital centers that are 
liable to be damaged in the handling of the growth. Nevertheless it 
is to be remembered that both Macewen and Parkin operated success- 
fully upon a cerebellar tumor. 

The symptomatic treatment of brain tumor by operation is always 
to be considered when the removal of it is out of the question. Tre- 
phining, withdrawing some of the fluid and thus lessening the intra- 
cranial pressure have afforded temporary relief of the headache, stu- 
por and optic neuritis. When symptoms are severe and blindness is 
threatened one can readily see the commendability of such a procedure, 
though the benefit may be only temporary. 

In some cases the ventricles have been tapped in the hope of re- 
lieving the pressure symptoms. The results have been very doubtful, 
however. The same is to be said of lumbar puncture, a most doubt- 
ful procedure. 

INTRACRANIAL ANEURISM. 

An aneurism is a variety of tumor, soft, pulsating, attached to a 
bloodvessel, and terminating usually in rupture and hemorrhage. In- 
tracranial aneurisms may be within the brain, on the minute terminal 
arterioles that penetrate its substance, or between the brain and the 
skull on the large arteries found there. The former are called miliary 
aneurisms, are small and produce no symptoms until they rupture and 
allow the blood to pour out into the brain substance. They are of 
interest chiefly in connection with intracranial hemorrhage, under 
which head they have been considered. The large aneurisms may be 
formed anywhere where there is a large vessel in the intracranial 
cavity. By far the greater number of them occur on the large arteries 
at the base of the brain. 

Etiology. — The causation of intracranial aneurisms is in the 
main the same as that of aneurismal dilatations elsewhere in the 
body. Men are more subject to the disease than women, in the pro- 
portion of about three to two. The reason for this is probably not an 
inherent difference between the sexes, but a difference in their modes 
of life. The greater tendency to exposure, strain and dissipation in 
men leads to a greater deterioration of the walls of their arteries. 
This is shown in another way when the age at which these aneurisms 
occur are considered. For instance, they all appear between the years 
of ten and sixty, and within this period the greater number show 
themselves during the first half or when exposure, strain and dissipa- 



THE NON-NEURONIC DISEASES 935 

tion are most rife. In some families there seems to run a slight in- 
heritance toward arterial disease. This has been mentioned before in 
connection with intracranial hemorrhage. The nature of this con- 
genital influence we know absolutely nothing about. It is an inheri- 
tance not of the disease itself but of the predisposition to the disease, 
a very important distinction to keep always in mind. With or with- 
out such a predisposition an aneurism may be initiated by various 
exciting causes chief of which are blows, shocks and other traumata to 
the head. 

The immediate cause of the dilatation is a diseased state oi the 
arterial walls. The muscular and elastic tissue is diminished and re- 
placed by a fibroid and otherwise degenerated tissue. Under the 
pulsations and pressure of the blood stream the wall distends but does 
not contract again as it should. In the course of time the bulging be- 
comes larger, more permanent and finally constitutes an aneurism with 
thin walls, pulsating and variable in shape. 

Primary degeneration, syphilis and emboli, especially when in- 
fected, are the chief factors in the production of the disease of the 
vascular walls. The first is largely an accompaniment of old age 
and with traumatism is perhaps the cause of most of the aneurisms 
in other parts of the body ; the second and third are conditions of early 
adult and middle life and are the principal elements in the produc- 
tion of intracranial dilatations. The primary degeneration may be 
-fibroid or atheromatous; even extensive fatty and calcareous break- 
down may be seen. Specific arteritis is a condition so well known 
that it need only be mentioned here. Emboli, especially infected em- 
boli, are the products of endocarditis. Minute vegetations break off 
from the diseased valves of the heart, float away to the brain on the 
blood current and finally become lodged at the bifurcation of some 
artery. Obstruction takes place, the vessel becomes closed and oblit- 
erated in front of the obstruction, inflamed and degenerated behind 
it. The cause of this inflammation is irritation and infection. These 
causes of the arterial disease explain clearly why the basilar and ver 
tebral system of vessels are so much more frequently affected in ad- 
vanced years while the anterior and middle cerebral-, especially the 
latter on the left side, are seen to be the choice site of the aneurism in 
earlier years. 

PATHOLOGY. — Scarcely more need be said upon the patholog) of 
this condition than what has been mentioned under tin etiology. The 
arteries that are afTected in the order of their frequency an- the mid 
die cerebral, basilar, internal carotid, anterior cerebral, posterior com 
municatingi anterior communicating, vertebral, posterior cerebral and 

inferior cerebellar. Those of tin- left side far outnumber thos< 

the right. Within tin- central ganglia or ventricles aneurism is i 
rare. 

Usually the swelling is single though a multiple condition ma\ 
obtain. Its histological attributes arc- the same as all aneurisms and 
need not be discussed here. In developing it compresses and mon 
less damages the neighboring brain tissue. Nerves in juxtaposition 

may also undergo destruction. Even tin- bone tis>iir maj be eroded 



93^ THE NON-NEURONIC DISEASES 

by its steady pressure. The presence of the tumor is generally rec- 
ognized by the symptoms of this collateral damage to bone, brain and 
nerve. 

After a time the aneurismal sac bursts and a superficial, com- 
pressing, severe hemorrhage occurs, the blood escaping in most cases 
into the membranes at the base of the brain. This hemorrhage may 
be continuous or intermittent, through a small or a large opening. The 
ventricles may become gradually filled with the outpouring blood, or 
the latter may tear or disintegrate its way into the brain matter. From 
the internal carotid it may burst into the cavernous sinus. 

Symptoms. — The symptoms of an intracranial aneurism are prac- 
tically those of a tumor. They are general and focal. The terminal 
hemorrhage has its own special symptomatology which is closely sim- 
ilar to that of meningeal apoplexy. Headache is of a pulsating char- 
acter, constant, intense and accompanied often by local tenderness in 
some spot. Vertigo, giddiness, vomiting, projectile in character, stu- 
por and occasional convulsions are all characteristic symptoms and 
are due to the general intracranial increase of pressure. Cranial 
nerve palsies are frequent, though optic neuritis is not common. The 
usual aneurismal murmur is not often produced by the intracranial 
variety of dilatation. It was noted in aneurism of the internal carotid 
and left vertebral arteries. So many conditions give rise to cranial 
murmurs that the symptom is not very valuable here for diagnostic 
purposes. A pulsating vascular murmur may be heard sometimes in 
cases of tumor located near and compressing a large artery. It may 
be noted in hydrocephalus, anaemia, rachitis, and even in perfectly 
healthy children. Exophthalmic goitre and neoplastic compression 
of the sympathetic nerve have provoked cephalic murmurs. 

These general symptoms are the offspring mostly of moderately 
large aneurisms. With them may be associated certain focal symp- 
toms indicating where the tumor is located. In small aneurisms it 
may rarely happen that slight focal symptoms are presented but no 
general manifestations. 

The localisation of an aneurism by means of its focal exhibitions 
follows the same general rules that the localization of an ordinary tu- 
mor follows. Motor and sensory disturbances should be carefully 
noted and compared with one another and their correlation with the 
areas of the brain should be made in accordance with the known facts 
of brain physiology. 

When the aneurism is in the internal carotid artery there is com- 
pression of the optic nerves, the oculomotor nerves, the olfactory and 
the trigeminus. The sight of one eye therefore fails, ptosis occurs 
on the same side, the sensibility of the eye is lost with all its usual 
consequences and the power of smelling is damaged. Hemiplegia may 
occur from the pressure backward on the crus cerebri. On the left 
side the speech center may be implicated with the production of motor 
aphasia. The free communication between the ophthalmic and facial 
veins usually quickly relieves what transient fullness may occur in 
the retinal veins from pressure on the cavernous sinus. Michel finds 
that the occasional optic neuritis that is seen is not due to compression 



THE NON-NEURONIC DISEASES 937 

but to extension of inflammation from the vicinity of the aneurism. 
When rupture takes place, as it does in a little less than half the cases, 
the cavernous sinus is invaded and a pulsating exophthalmus may 
result. 

Swellings on the anterior, middle and posterior cerebral arteries 
can be surmised from symptoms pointing to implication of the ad- 
jacent cortical centers. With the first, for instance, the symptoms are 
the same as those in aneurism of the internal carotid except for the 
involvement of the third nerve. Aneurism of the middle cerebral, or 
artery of the Sylvian fossa, provokes hemiplegic convulsions and 
speech disturbances especially. The cranial nerves are notably free 
from involvement. Being near the motor zone, Jacksonian symptoms, 
followed by monoplegia and hemiplegia, are the characteristic features. 
Sometimes they cause no outward evidences of their presence. About 
two-thirds of them rupture. A posterior cerebral aneurism is apt to 
compress the upper part of the pons, the crus cerebri temporo-sphe- 
noidal lobe, the third and sixth nerves. Alternating hemiplegia there- 
fore is to be expected. 

An enlargement of the anterior communicating artery produces, 
as a rule, no symptoms, because it is usually small and compres 
merely the inner sides of the frontal lobes. If it is large the olfactory 
and optic nerves may be affected. 

When the posterior communicating vessel is the seat of the dilata- 
tion hemianopsia may be produced by compression of the optic tract. 
The temporo-sphenoidal lobe and basal ganglia may be compressed. 
The third nerve is the one most commonly implicated. Hemiplegia 
is rare. 

Vertebral aneurisms do not often cause serious trouble. In fact 
the condition in these arteries is usually one of gradual extensive 
dilatation of the artery tharkthat of a typical aneurism and the symp- 
toms, such as they are, are notable for their slowly progressive char- 
acter. The symptoms are more or less similar to those- of basilar 
aneurism. 

The basilar artery is a frequent site of both aneurism and uniform 
dilatation. Its close proximity to the pons, the medulla and the c< 
bral crura indicates the possible symptomatology. The general symp- 
toms, especially the headache and vertigo, arc unusually pronounced. 
Pontile symptoms, such as alternating hemiplegia, upper cranial nerve 
involvement, and forced movements, occur when tin- swelling is high 
up. Bulbar symptoms with dysarthria, dysphagia, cardiac and respira- 
tory difficulties combined with hemiplegia appear when the enlai 
ment is lower down. Internal hydrocephalus occasionally occurs. I 
vulsions are rare. Occasional apoplectic attacks sometimes happen. 
About half the cases rupture. 

Cerebellar aneurisms are of no interest clinically. 

Prognosis. — An intracranial aneurism is a most dangero 
session. The greater number of those that have produced Sufficient 
symptoms to enable them to be diagnosed during life have soon< i 
later terminated by rupture. The duration of these enlargements 



93& THE NON-NEURONJC DISEASES 

ranges from a few weeks to six years. An occasional spontaneous 
cure has resulted from the filling of the sac with a clot; 

Treatment. — The dyscrasia that causes the disease in the walls 
of the arteries would seem to invite treatment but it is hardly to be 
expected that such treatment will modify an aneurism after it has once 
developed from such a vascular condition. Syphilitic history there- 
fore recommends the use of potassium iodide and mercury to prevent 
at least the extension of the disease in the arterial walls. Atheroma 
and other degenerative conditions may be attacked, but little real benefit 
will accrue thereby to the aneurism. The use of potassium iodide in 
moderate dosage, thirty or forty grains a day, has seemed to favor 
intra-aneurismal coagulation and spontaneous cure in a few instances. 
It should be tried. Ergot is useless and irrational. 

In the general regimen and mode of living everything should be 
done to avoid momentary or continuous increase in the intracranial 
blood pressure. Tight bands about the neck must be eschewed. Strain- 
ing at stool, giving way to passionate anger, coughing, running to 
catch a train, must not be permitted. Stimulants, like alcohol and 
coffee and tea, must be left alone. An even, quiet existence with a 
bland, nutritious dietary and little drink should be constantly main- 
tained. In sleeping the head should be elevated and in waking never 
extended or flexed on the body too far. 

Surgical measures have been tried for the cure of these aneurisms 
but without any very flattering results. Only in the rarest cases is 
the diagnosis sufficiently precise to cause surgery even to be thought 
of. Dilatations on the internal carotid have been diagnosed and the 
artery itself ligated with success. The vertebrals have been tied for 
a basilar aneurism. The risk of the operation, great as it is, is less 
than that of the aneurism. Lumbar puncture must be discountenanced. 
Most disastrous results have followed it. When rupture occurs, the 
physician's special services are at an end. 

HYDROCEPHALUS. 

This is another term representing merely a symptomatic con- 
dition, which, it is to be hoped, will ere long be allowed to follow 
the terms paralysis, apoplexy and Landry's paralysis in neurological 
nosology. It means merely dropsy of the brain, represents an accu- 
mulation of fluid and is the result of a considerable number of dis- 
eased conditions. It is never strictly a primary condition. Its imme- 
diate causes may be congenital, developmental anomalies, mechanical 
obstructions or meningeal inflammations. It is therefore both a con- 
genital and an acquired condition. From the standpoint of duration, 
the former is sometimes spoken of as chronic, and the latter as acute, 
hydrocephalus. This is clearly an injudicious use of adjectives, for 
acquired hydrocephalus may be chronic and a congenital form may run 
a rapid, acute course. On the basis of pathology, when the fluid occu- 
pies the ventricles, the hydrocephalus is said to be internal; when it 
is outside of the brain in the subdural space it is spoken of as external. 
Internal hydrocephalus has a varied etiology, as will be seen later on. 



THE NON-NEURONIC DISEASES 

External hydrocephalus, or hydrocephalus ex vacuo, is seen in senile 
conditions, atrophy of the brain, hemorrhages, encephalomalacia and 
sclerotic conditions, in cancer and other cachetic diseases, in chronic 
nephritis, chronic alcoholism, rickets, meningeal cysts and other 
chronic troubles and pathological residua. This, of course, is not a 
true dropsy, but rather a pathological, secondary effusion. 

It will be practically convenient, though somewhat arbitrary. t<» 
discuss the malady under the three subheads, as Osier does. Serous 
Meningitis. Congenital Hydrocephalus and Acquired Chronic Hydro- 
cephalus. These are all internal types of hydrocephalus. The ex- 
ternal types might be added as a fourth subhead, but as they are merely 
symptomatic of so many different disease states, their discussion would 
be an unnecessary recapitulation of what has been said under the head 
of these diseases elsewhere. 

Serous Meningitis. — This is a form of internal hydrocephalus 
whose pathogenesis is obscure. Quincke has studied it very closely 
and arrived at the conclusion that it is due to a simple serous inflam- 
mation of the meninges of the ventricles with effusion, analogous to 
serous pleuritis. It is thus an ependymitis and one wonders at the 
significance of the name sometimes applied to it, idiopathic internal 
hydrocephalus. So much doubt is there in regard to its inflammatory 
nature that Quincke himself likens the process to that of angioneurotic 
oedema of the skin, and speaks of it as an angioneurotic hydro- 
cephalus. It is easy to understand the secondary nature of the effusion 
in this form of ventricular dropsy but the cause and nature of the 
primary trouble in the ependyma or related structures are far from 
being established. In acute cases the ependyma exhibits no abnormal 
appearance whatever; in the chronic cases it is rough and thickened. 
In some cases distinct signs of inflammation appear, not only in the 
intracerebral pia, the choroid plexus, but in the cortical pia also. In 
the latter case there is also an external hydrocephalus. < me hypoth< 
though far from being a satisfactory one. attributes the ventricular 
effusion to the closure of the foramen of Magendie by the simple 
basal meningitis. The disease occurs almost a> frequently, however, 
without any indications of meningitis, internal or external. 

The exudate is believed to arise chiefly from the choroid plexus 
and the walls of the ventricles. It does not materially differ from 
the normal cerebrospinal fluid. If its specific gravit) should be- ab 
1009, w * tn albumin present in larger amount than two per thousand, 
tumor or stasis is more likely to be the original cause of the drop 
In some cases it has been thought that tin- entire disease owed 
inception to a trauma, mental strain, alcoholism. various acute ini 
tious diseases, purulent otitis and toxaemia. 

It is quite impossible, in our present state of knowled 
rately classify this form of hydrocephalus. It seems to occur as both 
a congenital and acquired affection. It appears in children but adults 
are more frequently attacked by it. It runs both an acute and a chronic 
course. In its essential origin it is not alv decide 

whether it is a primary or a secondary manifestation. It is usually 
internal though it may be accompanied b> an external dropsy. In 



94° THE NON-NEURONIC DISEASES 

some cases inflammation, in others mechanical obstruction, and appa- 
rently in a considerable number of cases, a developmental functional 
defect may be at the bottom of it. No name, beyond hydrocephalus, 
that has hitherto been given to it is strictly correct. 

Symptomatically there seem to be various well-marked types of 
the affection. As an acute trouble it closely resembles sometimes either 
a purulent or a tuberculous meningitis. It is not improbable that some 
reported cures of the latter disease have been cases of this form of 
hydrocephalus. Headache is present. There are signs of increased 
intracranial pressure. The discs are choked. The pulse is retarded. 
The neck is retracted. The fever is slight, inconstant and usually ab- 
sent. It may be present at first and then disappear. In some cases 
loss of the knee-jerk has been observed. Lumbar puncture may aid 
much in the making of a differential diagnosis. In meningitis of the 
purulent or tuberculous type, the cephalalgia is apt to be keener, the 
retraction of the neck more forcible and all the other well known 
signs, such as occur in the pupils, in Kernig's phenomena, in the stu- 
por, in the gait, more pronounced. Excessive visual disturbance points 
rather to the hydrocephalic condition. Bacilli in the cerebrospinal fluid 
and the discovery of tuberculosis or local infection elsewhere may 
clinch the diagnosis. Sometimes a differential diagnosis is absolutely 
impossible. This acute hydrocephalus usually recovers completely or 
partially in a few weeks or passes into a chronic form of the trouble. 

When it has become chronic, this form of cerebral dropsy is very 
liable to be mistaken for tumor of the* brain and cause a false notion 
of a cure of the latter when the symptoms have disappeared. Like 
tumor it provokes both general and focal symptoms. The former in- 
clude intense headache, slight fever, vomiting, vertiginous attacks, 
somnolence, stupor, delirium, retardation and acceleration of the pulse. 
Optic neuritis with choked disc, and later on atrophy, are very fre- 
quent manifestations. Exophthalmos may occur. Hemianopsia, local 
spasms, muscular rigidity, temporary monoplegias and hemiplegias and 
signs of cranial nerve involvement are among the more important focal 
symptoms. As the clinical presentations of this hydrocephalus have 
the remarkable property of undergoing exacerbations and varying 
degrees of intensity from day to day, they can be distinguished from the 
progressive symptoms of tumor. Moreover the hydrocephalic skull 
is in evidence in most of the cases, showing that though the cases 
occur mostly in adults in this chronic form of the trouble there has 
been all along a congenital predisposition. This, of course, is not the 
case in tumor. 

The diagnosis of this hydrocephalus rests primarily upon its 
pressure symptoms, its characteristic remissions and intermissions, its 
temporary focal exhibitions or absence of them, its congenital hydro- 
cephalic predisposition, and its cranial nerve involvements. The nor- 
mal character of the cerebrospinal fluid as distinguished from the 
albuminous fluid of tumor is helpful in making a differentiation in some 
cases. In children the diagnosis is less difficult than in adults because 
the hydrocephalic deformities of the head are more prominent in them. 
The total clinical picture, studied in every possible way and with all 



THE NON-NEURONIC DISEASES 941 

possible aids to examination, must form the basis for the diagnosis 
of so obscure a disease rather than one or two symptoms only. This 
picture must be both broadly and minutely contrasted with that pre- 
sented by intracranial tumor, purulent meningitis, tuberculous menin- 
gitis and some other diseases. Even then, unfortunately, the diagnosis 
cannot be made positively in a good many cases. 

Recovery frequently follows, in these cases, many weeks of suf- 
fering. In spite of the presence of intense headache, vomiting, stu- 
por and optic neuritis, mercurial treatment has eventuated in a com- 
plete cure after several weeks or months. The course of the disease 
is always remittent. Sometimes it becomes chronic and in children 
cannot be distinguished from the ordinary form of congenital hydro- 
cephalus. Death occurs rather infrequently. 

Here could be discussed logically some cases of acquired hydro- 
cephalus that run a course, and in many respect are, similar to 
Quincke's type of the disease. This is especially true of some of the 
cases of secondary external hydrocephalus. One form of the latter 
has already been referred to, as it is sometimes regarded as primary 
and aligned with similar cases of so-called angioneurotic hydro- 
cephalus. Most of the cases, however, are associated with atrophy 
of the brain, which is supposed to cause a vacuum with resulting effu- 
sion between the brain and the skull. Hence the name hydrocephalus 
ex vacuo. Other cases, both internal and external, are attributed to 
trauma, insolation, congestion, obstruction of the venae Galeni. of the 
aqueduct of Sylvius, or of the foramen of Monroe by various neo- 
plasms, cysticerci, cicatrices, etc. Purulent and tuberculous menin- 
gitis after the same manner may be accompanied by dropsy of the 
brain, as also may phthisis, nephritis, marasmus and various cachexias. 
In many of these cases a slight hydrocephalus, or at least hydrocephalic 
tendency, has probably existed from birth and the causes mentioned 
have only awakened it from its latency. At all events the cases are 
not in any way distinctive and are of no special clinical interest be- 
yond that of the disease with which the hydrocehalus is associated. 

Acquired Chronic Hydrocephalus. — This then is the affection to 
which what has just been said is largely applicable. It is always sec- 
ondary, even in what is sometimes called the primary or idiopathic 
form which is in great need of thorough pathological reinvestigation. 
Mechanical obstructions and meningitis are the primary cause of the 
trouble in nearly all of the cases. All of the etiological factors in this 
form of the trouble take their cue from tin- etiology of the primary 
cause. In adults, of course, the head will not be enlarged though there 
may be an intense degree of dropsy present. In children the skull may 
and usually does undergo early and steady expansion. Even in them 
the enlargement may not hi- commensurate with tin- severity of the 
other symptoms. The brain substance may he so compressed and 
attenuated that the ventricles are enormously distended while the gen- 
eral size of the head remains about normal. The external appearances 
are often the same in children as they are in the ordinary congenital 
type of the disease. The symptoms are extremely numerous and varia- 
ble, especially in the adult. They art- those chiefly of intracranial 



94 2 THE NON-NEURONIC DISEASES 

pressure. In children idiocy and imbecility occur, in adults stupor, 
delirium and maniacal outbreaks. In rare instances acquired, men- 
ingitic external hydrocephalus is sacculated on account of the ad- 
hesions between the pia and the dura. The condition is a veritable 
meningeal cyst. The limited pressure upon the brain by such cysts 
may give rise to pronounced pressure focal symptoms. There is 
hardly any need of dwelling here upon the headache, the vertigo and 
vomiting, the optic neuritis, the cranial nerve palsies, the tremors, the 
spasms, the stupor and coma that are observed in these cases. Tumor 
of the brain probably causes the greatest difficulty in the differential 
diagnosis. (See the discussion of this in the preceding paragraphs 
under the head of internal meningitic hydrocephalus.) 

Congenital Hydrocephalus. — This is the typical form of the trou- 
ble, the most common and the one generally referred to when the term 
hydrocephalus alone is used. It is practically always internal. Its 
course may be acute or chronic. The etiology of the disease is ex- 
ceedingly obscure. It seems to be more than merely congenital at 
times. The appearance of the condition in several members of the 
same family and in two and three successive generations indicate a 
purely hereditary influence. In conjunction with this fact it is sug- 
gestive that various cachexias, alcoholism and syphilis have been reck- 
oned among its etological incidents. I have seen it in syphilitic fam- 
ilies. Oppenheim has several times observed a moderate hydro- 
cephalus in hereditary syphilitics with severe symptoms coming on 
later in life. Of the direct prenatal causes that are responsible for it 
we know nothing. Psychic excitement and traumata sustained by trie 
mother while she is carrying the fcetus, uterine disease, etc., are some 
of the hypothetical causes that have been enumerated. 

The pathology of the disease is capable of being described but 
its pathogenesis is still completely in the dark. The essential fact 
in its pathology is the excessive accumulation of fluid in the ventricles. 
The fluid varies but little from the normal. It is clear, colorless, has a 
specific gravity of from iooi to 1009 and contains a small and variable 
amount of albumin, a slight quantity of sodium chloride, occasionally 
some urea, cholesterin and other unimportant substances. The amount 
varies in different cases from a few ounces to several pints. It usually 
distends all of the ventricles, particularly the lateral. It may be lim- 
ited to particular ventricles by the mechanical obstruction or inflam- 
matory closure of the inter-communicating ducts. 

The other pathological findings are the direct result of the con- 
stant pressure and distention exerted by the fluid. The most remark- 
able of these is the atrophy and wasting, the thinning out and displace- 
ment of the brain substance. It is astounding at times to what an ex- 
tent the wall of the hemispheres can be reduced. Both compression 
and stretching is the cause of this. The entire brain may seem to be 
transformed into a huge cavity inclosed by walls not more than a few 
millimeters thick. It is said that Cardinal, Brigfht's famous patient, 
lived to be twenty-nine years of age, with a hydrocephalic head per- 
fectly translucent when the sun was shining behind it. The convolu- 
tions and sulci, of course, are obliterated. The corpus callosum is car- 



THE NON-NEURONIC DISEASES 943 

ried upwards, the central ganglia are flattened out and the floor of the 
third ventricle bulges beneath. Sometimes the convolutions are only 
partially obliterated and the basal ganglia are found at the bottom of 
the sac. The skull is uniformly enlarged in correspondence with the 
cerebral distention. The falx is stretched and the tentorium is elevated 
anteriorly. The space beneath the tentorium is increased in size and is 
incompletely filled by the cerebellum. Either fluid or connective tissue 
may occupy the space between the cerebellum and the membranes. 
The choroid plexuses are thickened and seem to have been inflamed 
while the ventricular ependyma is often finely granular in appearance 
and sodden. 

The external appearance of the head is striking and characteris- 
tic. It is uniformly enlarged with a strong tendency towards being 
dolichocephalic or boat-shaped. As the face remains small the front 
part of the cranium hangs over it like a beetling brow. The promi- 
nences are all enlarged, smooth and rounded. A balloon-like appear- 
ance is thus strikingly given to the upper part of the head. The cir- 
cumference, measuring normally in the newborn about thirty-five to 
forty centimeters, may reach the enormous size of a hundred and 
sixty-seven centimeters. The bones are thin, the sutures gaping, the 
fontanelles large and bulging. On account of the downward pressure 
on the orbital plates, the eyeballs protrude and the eyes are directed 
downward and partially covered by the lower lids. Wormian bones 
sometimes develop in the sutures of the skull. The entire shape of 
the head is such that it can be readily distinguished from the square- 
shaped, angular, rachitic head. Ofttimes developmental defects are 
seen in other parts of the body, such as encephalocele, hare-lip, spina 
bifida, club-foot and a general condition of dwarfism. Albinism has 
been noted. 

In addition to the physical appearance of the child, other symp- 
toms enter into the composition of the clinical picture of this disease. 
The head may be so large as to obstruct the act of parturition ; very 
often, however, it does not begin to be very noticeable until the child 
is several weeks or months old. From that time on there is then a 
steady increase in the size of the cranium. The veins appear prom- 
inently beneath the skin. The hair fails to grow. Auscultation en- 
ables one to detect a brain murmur and percussion reveals a fluctua- 
tion wave. 

Idiocy and imbecility is the lot of these children. The intellect is 
weak even in the mildest cases and the speech slowly acquired. Rarely 
a hydrocephalic child will be bright mentally; the disease becomes ar- 
rested; and adult life may be reached with normal faculties. In still 
rarer instances the mental faculties have been retained with a high de- 
gree °f hydrocephalus. 

General spasms and epileptiform convulsions are common. The 
head cannot be held erect, partly on account of it> weight, partly on 
account of the weakness of the muscles. The voluntary movements 
are never learned. SO that the child carries his limbs about in an awk- 
ward manner. The legs are usually somewhat spastic, causing ;i de- 
cided difncultv in the rait. Many children never learn to walk. < Mhers 



944 



THE NON-NEURONIC DISEASES 



wabble and shift about in the most ungainly way. Incontinence of 
urine and feces is a mental rather than a motor trouble. Choked disc 

FIGURE 203. 




Hydrocephalus. 



Fitch's case. 



and optic atrophy are very frequent accompaniments of the disease, 
caused, of course, by the pressure upon the optic nerves. Sensation 
is not as often affected as motility and seldom are the cranial nerves 



THE NON-NEURONIC DISEASES 



945 



except the optic, implicated. Profound stupor, fever, vomiting and 
coma may herald the end. 

FIGURE 204. 




I [ydrocephalus. 

The outlook for these children is bad. They usually die- within 
the first four or five years of life. This is a blessing iu disguise if the 
case is a severe one at all, for the prospect <>t idiocy, n life contin 



946 



Till-: .\ON-NEURONIC DISEASES 



is strong. In some cases evacuation of the fluid has occurred through 
a spontaneous rupture, with amelioration of the symptoms. In the 

FIGURE 205. 




Hydrocephalus. 

mildest cases life has been prolonged to old age, the disease having 
doubtless become permanently arrested. The prognosis of hydro- 
cephalus is therefore always serious and full of uncertainty. 



THE NON-NEURONIC DISEASES 947 

Treatment. — The treatment of hydrocephalus of all forms is 
far from satisfactory. In the acute and chronic acquired forms it is 
more hopeful than in the congenital. It is always uncertain, however, 
how much of the recovery was due to the therapeutic measures insti- 
tuted and how much to the natural events of the disease. In the ac- 
quired types of the trouble, treatment should always be directed, so 
far as possible, to the underlying primary disease. Quincke advises 
mercurial treatment in all of these cases, especially the internal men- 
ingitic cases, whether a history of syphilis be obtainable or not. Medi- 
cines cannot remove the fluid. Purgatives and diuretics, so much 
vaunted in earlier days, accomplish practically nothing, and are often 
dangerous if used with necessary vigor in the weakened state of these 
patients. 

Surgical measures, therefore, as a rule, are our only resort and 
these are not very promising. They consist of stead}- compression of 
the head, partial withdrawal of the ventricular and spinal fluid by punc- 
ture, violent revulsive measures and ventricular drainage. 

It does not seem very rational to transfer the pressure of the ac- 
cumulating fluid from the skull around it to the brain within it by ex- 
ternal compression of the head. And yet that is a practice that is 
honored both by age and by a few apparent cures. Trousseau, and 
others to-day. recommend the application of strips of adhesive pias- 
ter up over the vertex from one mastoid process to the other, from the 
nose to the occipit, and then in circles around the head horizontally. 
The case must be closely watched and the strips removed upon the 
first indication of undue pressure upon the brain. It was first hoped 
that this would favor the reabsorption of the fluid. Then a check to 
the enlargement of the head was all that was anticipated. Neither of 
these results, however, are accomplished, whereas an increase in the 
symptoms of compression almost always lakes place. West recom- 
mends the use of a broad elastic band instead of the diachylon plaster. 
He, with most other clinicians, however, recognizes the general futil- 
ity of this method of treatment. 

Withdrawal of the fluid by puncture is the most direct, but also 
the most dangerous, mode of attempting relief. Hippocrates re-com- 
mended puncture of the ventricles. Simple puncture under the strict- 
est kind of antisepsis, withdrawal of not more than an ounce of fluid 
at a time, and the operation not repeated at too close or frequent in- 
tervals, have in a few instances seemed to have resulted in a cure- 
In sixty-three cases. Eienschen reported fifteen recoveries, twelve im- 
provements and twenty-four deaths. ( )ften the first operation is borne 
well but the second or third proves fatal. Puncture, with after- 
drainage, and puncture with iodine injections, seem to have been 
particularly dangerous. The insertion of the aspirating needle or tro- 
car is usually best made at the outer angle of the anterior fontanelle. 

Much safer, though slower in action, is puncture of the sub- 
arachnoid sac of the spine between the third and fourth lumbar ver- 
tebrae. This measure has proved to be both curative and palliative, 
especially in acquired hydrocephalus. 

Revulsive measures consist of the use of the set<>n. inunctions 



948 THE NO N- NEURONIC DISEASES 

with ointments of tartar emetic and even the once so popular appli- 
cation of spirit of turpentine freely to the scalp and then setting it on 
fire. These heroic measures unfortunately do not cure and only too 
often fail to relieve. It must be admitted, to the chagrin of both 
medicine and surgery, that the treatment of hydrocephalus is not a 
brilliant success and only too often nature and a laissez-faire policy 
accomplish about as much as do science and art. 

DISEASES OF THE PONS VAROLII AND MEDULLA 
OBLONGATA. 

It is not necessary to give a minute description of the pons and 
medulla here, for the main points in their anatomy have been touched 

FIGURE 206. 
pc ft !'* 




ale 

Diagrammatic representation of a section of the medulla at the level of the 
decussation of the pyramidal tracts: fp., posterior fissure; f, anterior fissure; 
p, crossing of the pyramidal tracts; fg, fasciculus gracilis; a, anterior horn; 
pc, posterior horn; R, substantia gelatinosa of Rolando; 1, lateral column; ac, 
anterior column; ap, pyramid. (From Quain.) 

upon in the earlier accounts of the anatomy of the brain and of the 
neuronic architecture of the nervous system. 

The medulla is but an upward extension of the spinal cord. Its 
tracts and gray matter are the same, with but a slight alteration in 
their relative positions. Usually that part is called the medulla which 
extends from the edge of the foramen magnum up to the lower border 
of the pons. As the tracts of the medulla continue to course on up- 
wards to be prolonged into the crura cerebri, they are embraced ven- 
trally and crossed transversely by the great commissural fibres of the 
cerebellum. These transverse fibres and all that lies behind them is 
known in gross anatomy as the pons varolii. 

It is better to regard the upward extension of the medulla, lying 
behind the transverse tracts of the pons, as the preoblongata. What 
is commonly called in anatomy the medulla may then well be called 
the postoblongata. Behind the preoblongata is the fourth ventricle, 
with the aqueduct of Sylvius above leading to the third ventricle. 



THE XOX-XEUROXIC DISEASES 



949 



There are three important facts to be noted in connection with 
the rearrangement of the spinal cord tracts in their upward extension 
into the medulla. The first is that there is a sort of an antero-posterior 
flattening out of the cord, with a gradual posterior displacement of the 
anterior parts thereof. The posterior columns separate, V-shape, and 
continue on up as the restiform bodies and inferior cerebellar peduncles. 
The central canal of the cord opens out into the fourth ventricle, which 
is bounded above laterally by the superior cerebellar peduncles. The 
central gray matter and anterior horns of the cord sink backwards until, 
with the widely separated remains of the posterior horns, they form a 
plate of gray matter just beneath the floor of the fourth ventricle. At 



FIGURE 207. 



TcM. — 




Section op the medulla 
oblongata in the region of the 
superior pyramidal decussation. 
(Schwalbe.) •£ 

a.m./., anterior median fissure ; 
f.a., superficial arciform fibres emerg- 
ing from the fissure ; py. , pyramid ; 
n.ar. y nucleus of the arciform fibres ; 
f.a'., deep arciform fibres becoming 
superficial ; 0., lower end of olivary 
nucleus ; o\, accessory olivary nucleus ; 
n.l., nucleus lateralis ; f.r., formatio 
reticularis ;/.a. 2 , arciform fibres pro- 
ceeding from formatio reticularis ; g., 
substantia gelatinosa of Rolando ; 
a. V., ascending root of fifth nerve ; 
n.c, nucleus cuneatus ; n.c'., external 
cuneate nucleus ; f.c, funiculus cu- 
neatus ; n.g., nucleus gracilis ; f.g., 
funiculus gracilis; p.m./., posterior 
median fissure; c.c, central canal 
surrounded by grey matter, in which 
are, n.XT. f nucleus of the spinal 
accessory, and, n.XIL, nucleus of the 
hypoglossal : s.d. f superior pyramidal 
decussation. 



the top of the posterior columns an expansion of gray matter becomes 
the nuclei of the posterior columns. 

The second great change in the medulla to be noted in relation to 
the cord tracts is that the pyramidal tracts course ventrally and decus- 
sate in the well-known decussation of the pyramids. 

The third change is that the sensory tracts in large part decuss 
in the fillet. 

With the aid of the accompanying diagrams and a knowledge of 
the gross anatomy, the reader can easil) trace every pathway and gray 
deposit in the spinal cord up into the medullar. The apparent con 
fusion is caused merely by their rearrangement and not by an) essen 
tial change. 

The cranial nuclei arc the special points of interest in the medulla 
in clinical neurology. These nuclei arc tin- cause of the special symp- 
tomatology of medullary diseases. Th< y arc all in the gra) matter 
making up the floor of the fourth ventricle and the aqueduct of Sylvius. 



950 



THE N0N-NEUR0NIC DISEASES 



They are the remains of the anterior and posterior horns and central 
gray matter of the spinal cord. 

The Figure 175 illustrates more accurately than any long 
description can the relative positions of these nuclei. Being but the 
upward extension of the gray matter of the cord, they are liable to the 
same sort of disease processes that the latter is. They may undergo 
primary and secondary degeneration and be subject to the distinctive 
effects of hemorrhage, inflammation, compression, etc. In this respect 
medullary diseases differ in nowise from spinal cord affections. 

The symptoms of disease of the medulla and pons are both general 



7i.am. 



FIGURE 208. 

Section op the me- 
dulla OBLONGATA AT ABOUT THE 
MIDDLE OP THE OLIVARY BODY. 

(Schwalbe.) ± 

f.l.a., anterior median fissure ; 
n.ar., nucleus arciformis ; p., 
pyramid; XII., bundle of hypo- 
glossal nerve emerging from the 
surface ; at b, it is seen coursing 
between the pyramid and the 
olivary nucleus, o. ; f.a.e., exter- 
nal arciform fibres ; n.l., nucleus 
lateralis; a., arciform fibres 
passing towards restiform body 
partly through the substantia gel- 
atinosa, <j. , partly superficial to 
the ascending root of the 5th 
nerve, a. V. ; X, bundle of vagus 
root, emerging ; f.r., formatio re- 
ticularis ; c.r., corpus restiforme, 
beginning to be formed, chiefly 
by arciform fibres, superficial and 
deep ; n.c, nucleus cuneatus ; 
n.y., nucleus gracilis ; t., attach- 
ment of the ligula : f.a. , funiculus 
solitarius ; n.X. , u. X'. , two parts 

of the vagus nucleus ; n.XIL, hypoglossal nucleus ; n.z., nucleus of the funiculus teres : 
n.am., nucleus ambiguus ; r., raphe ; A., continuation of anterior column of cord ; ^,o", 
accessory olivary nuclei ; p.o, pedunculus olivae. 




and focal. The former are the same as they are in similar trouble in 
other parts of the nervous system. The focal symptoms arc the great 
dominant feature in bulbar and pontile disease. These have been de- 
tailed elsewhere under the head of cerebral localization and symptoms 
of disease of the brain. 

Among the cranial nerves there are two quite distinct groups — 
namely, those that move the eyeball and those that innervate the mus- 
cles about the orifice of the alimentary and respiratory canals. The 
nuclei of the third, fourth and sixth nerves of the first group are scat- 
tered along the floor of the aqueduct of Sylvius. When they undergo 
primary degeneration the disease is known as degenerative ophthal- 
moplegia, described elsewhere. Sometimes they are made the seat of 
a hemorrhagic inflammation, which is supposed to be of infectious 
origin or toxic, and analogous to the same process that takes place in 



THE N0N- NEURONIC DISEASES 



95 ^ 



acute anterior poliomyelitis lower down in the cord. This is Wernicke's 
acute superior polioencephalitis. 

When primary degeneration attacks the lower group of nuclei the 




FIGURE 209. 




FIGURE 210. 



Figure 209, section of the medulla oblongata just above the pyramidal decussa- 
tion. Figure 210, section through the pyramidal decussation. I Mter Jakob.) 

condition is known as chronic or progressive bulbar paralysis. It may 
continue as an isolated affection, but more generally it is associated 
with progressive muscular atrophy, there being no fixed rule oi pr< 



95 2 THE NON-NEURONIC DISEASES 

dence in regard to the appearance of the bulbar or the spinal symp- 
toms. I have described this also elsewhere. This second group of 
nuclei, like the first, can also be subject to an acute hemorrhagic in- 
flammatory process, a condition which is sometimes called acute in- 
ferior polioencephalitis. 

These are all forms of bulbar paralysis. They are essentially dis- 
eases of the lower motor neurones, with all the characteristics that 
belong to such diseases in regard to atrophy, reflex action and elec- 
trical response. They are homologous to the poliomyelitic affections. 
The paralysis is flaccid and shows a tendency to pick out special mus- 
cles. Typical bulbar palsy is bilateral. Bulbar symptoms may, how- 
ever, occur unilaterally or even in the distribution of a single cranial 
nerve. Of course, in the last case, it is impossible to differentiate a 
neuritic from a nuclear palsy. A pseud o -bulbar palsy may be observed 
when a bilateral lesion implicates the cortical centers that correspond 
to the medullary nuclei. Under these circumstances the disease being 
in the upper motor neurones, the paralysis will be of the spastic type 
with increase of reflex actions and absence of atrophy and electrical 
changes. 

APOPLECTIFORM BULBAR PARALYSIS. 

Cases of a symmetrical bulbar palsy of sudden onset have been 
seen. They differ from the typical form of the disease in their 
apoplectiform and non-progressive character. . They occur in the later 
periods of life when there is beginning arterial degeneration. Younger 
persons have manifested the same condition as the result of trauma. 

The onset of the symptoms are sudden; usually without loss of 
consciousness; and with vomiting and vertigo. At first there may 
be motor and sensory disturbances in the limbs, but these quickly pass 
away and leave only the glosso-labio-laryngeal palsy. This even may 
improve for a time ; but finally the condition becomes stationary and 
may remain so for years. Late degeneration takes place and then the 
disease assumes all the characteristics of the progressive type of the 
disease. Perfect bilaterality does not always obtain in the symptoms. 
The weakness will be more marked on one side than on the other, 
or in certain muscles more than in others. 

In these cases, as in typical progressive bulbar palsy, there is 
dysarthria or anarthria, difficult deglutition and embarrassed respira- 
tion and voice production. 

The pathology of these cases is obscure, though it is probable that 
there is embolic obstruction in or near the middle line. In a case re- 
ported by Gowers in which there was no atrophy and no loss of elec- 
trical irritability — i. e., no evidence of damage of the nuclei themselves 
— it was surmised that the paths from the hemispheres were injuied 
just above the nuclei, near their decussation. The close commissural 
connection between the nuclei may easily account for the occasional 
appearance of bilateral symptoms from a unilateral lesion. 

The diagnosis of these cases is not difficult if the suddenness and 
complete bulbar picture are present. Mere focal lesions that damage 



THE NON-NEURONIC DISEASES 953 

suddenly this or that nucleus are not to be confounded with this 
disease. 

Pseudo-bulbar paralysis may at times closely simulate this affec- 
tion and cause serious mistakes in diagnosis. In these cases the lesion 
has for the most part been in the central ganglia. Both hemispheres 
were affected, but not simultaneously. The bulbar picture usually 
appeared after the second stroke, which completed the bilaterality of 
the lesion. 

In rare cases of pseudo-bulbar paralysis there have not been two 
successive apoplectiform attacks. These cases are extremely difficult 
to diagnose properly at times. The lenticular nucleus has been par- 
ticularly frequently the seat of the lesion. It has appeared elsewhere, 
however. The proper explanation of these cases is not yet forth- 
coming. 

There is an infantile form of pseudo-bulbar paralysis. 

The prognosis of these apoplectiform types of bulbar palsy is ex- 
ceedingly serious. Life is constantly in clanger. Xot being a primary 
degenerative disease, the later outlook is better here than it is in the 
typical progressive type of the disease. Sometimes much improvement 
occurs and complete recoveries have been several times recorded. If 
after a month there is no more improvement observed, it is probable 
that none will occur. 

The treatment is the same as that for intracranial embolism de- 
scribed in another part of the book. 

Bulbar palsy of a slow type may be due to compression from a 
tumor or aneurism. There is nothing distinctive about it. I have 
mentioned it when treating of intracranial tumors. 

Myasthenia gravis, which by some is called asthenic bulbar paraly- 
sis, is discussed in detail among the neuronic diseases of the lower 
motor segment. 

There is a hereditary and familial form of progressive bulbar 
paralysis, described by Fazio, Charcot, Londe and others, that rep- 
resents something more than a mere phase of progressive muscular 
atrophy as the common form of progressive bulbar paralysis does. In 
these cases the parents have been blood-relatives and the children have 
shown the disease. The physical stigmata of degeneracy are usually 
well marked in them. The atrophic paralysis usually begins in the 
upper facial area, continues there along with the involvement of the 
lower area and thus distinguishes these cases from the ordinary forms 
of the disease. Ptosis also occurs in these cases, showing the involve- 
ment of the third nerve nuclei. The extremities arc not implicated. 
There are other features about these cases that seem to distinguish 
them from the adult type of the trouble. It is supposed that there 
is a polioencephalitis underlying them. They seem to hi* more nearly 
related to the mysterious congenital ocular and facial palsies than 
to anything else, and are to be regarded in the light of developmental 
anomalies. Other forms of hereditary disease with bulbar symptoms 
have been observed, but little is known of their anatomical baa 

The pons is the seat of small focal lesions at times. There local- 
ization diagnosis is merely the application of the knowledge of anatomy. 



954 THE NON-NEURONIC DISEASES 

Small hemorrhages, spots of softening and tumor may occur here as 
elsewhere. Involvement of the cortico-spinal tracts, the formatio 
reticularis and the roots of the fifth nerve constitutes the prominent 
features of pontile symptomatology. 

In pontile lesions situated ventral ly, the damage to the pyramidal 
tracts dominates the clinical picture. This gives a uniform side to it. 
The other side of the picture will vary according as the lesion is in 
the upper (frontad) or lower (caudad) part of the pons. The pyra- 
midal tracts are from the cortex and distribute fibres to the cranial 
nuclei, as well as continuing on down into the cord. As we know, 
these tracts decussate ; those fibres to the cranial nuclei crossing above 
and those to the limbs crossing in the pyramids. If the lesion should 
be in the upper part of the pons, above a line drawn approximately 
through the points of emergence of the fifth nerves and involve the 
pyramidal fibres for the trigeminal, abducens and facial nerves before 
their decussation, the paralysis of the face and extremities will be on the 
same side of the body, but on the opposite side from that of the lesion. 
If, however, the lesion is below this line drawn through the trigeminal 
roots, after the pyramidal fibres for the above-named cranial nerves 
have decussated, the hemiplegia will be of the alternate or crossed type. 
The facial paralysis will be on the same side as the lesion, the paraly- 
sis of the extremities on the side opposite that of the lesion. In the 
former condition both facial and limb paralysis are of the pure central 
type ; in the latter condition the facial paralysis is of the peripheral 
type, while that of the limbs is of the central. 

Alternating anesthesia is occasionally met with in pontile lesions. 
According to Starr, a unilateral anaesthesia of the face (not due to 
trigeminal neuritis or to a cortical lesion) is indicative of a lesion in 
the medulla or pons, in the outer third of the formatio reticularis. If 
the lesion is high up (cephalad) in the pons, the anaesthesia will be on 
the opposite side; if the lesion is low down (caudad) in the pons or 
in the medulla, the anaesthesia will be on the same side. 

If anaesthesia occurs in the limbs and is not due to a cerebral 
lesion, the site of the trouble is in the medulla or pons, in the inner 
two-thirds of the formatio reticularis and on the side opposite that of 
the anaesthesia. Of course, it may be in the spinal cord. 

A lesion below the point of union of the ascending and descending 
roots of the fifth nerve and affecting the entire lateral extent of the 
formatio reticularis, will cause anaesthesia of one side of the face and 
of the limbs of the opposite side. 

If the face and limbs of the same side are anaesthetic, the lesion 
is frontad of the point of union of the ascending and descending roots 
of the fifth nerve in the pons. 

DISEASES OF THE CEREBELLUM. 

The anatomy and physiology of the cerebellum have been de- 
scribed with the brain at the head of this section. The results of ex- 
perimentation and pathological observation in regard to cerebellar 
lesions do not exactly coincide. Our knowledge of this part of the 



THE NON-NEURONJC DISEASES 955 

brain is incomplete. The clinical picture is usually confused by the 
symptoms of intracranial pressure, which symptoms may be due to 
parts entirely away from the cerebellum. 

According to Russell, experimental ablation of one half of the 
organ, exclusive of the middle lobe, results in incoordination, rotation. 
Jittibatwn, reeling, a characteristic attitude, disturbed reflexes, muscular 
rigidity and convulsions, motor paresis and ocular defects. These have 
all been seen as the result of disease in man. Just how much of the 
symptomatology is due in man to implication of the middle lobe of the 
cerebellum and pressure upon the medulla and the great tracts running 
through the medulla it is not easy to say. It is usually considered that 
a lesion of the cerebellar hemispheres in man that does not compress 
the middle lobe or medulla gives rise to no symptoms whereby it can 
be recognized. There are certainly no localizing signs. 

The reeling gait of the disease of the middle lobe of the little 
brain is almost pathognomonic. The patient finds it difficult to stand 
and every step is accompanied by unsteadiness, like that of a drunken 
person. It is almost impossible to maintain equilibrium. The walk is 
zigzag. Occasionally the movements of the arms are jerky. The gait 
is sometimes spoken of as ataxic, but it is not like the irregular ataxic 
gait of tabes, though the progression in tabes may sometimes approach 
in appearance the progression of cerebellar disease. In the latter it is 
distinctly reeling, oscillatory, unsteady and due to a distinct loss of 
the sense of equilibrium. This symptom may be produced by disease 
of the lateral hemisphere that compresses the middle lobe. 

Closely associated with this symptom are vomiting and vertigo. 
They are very common signs, though they are not of much value as 
localizing signs, since they occur in many other intracranial troubles. 
The vomiting is of the pure cerebral, projectile type. The vertigo is in 
no way distinctive. They occur only with irritative and compressing 
lesions and hence are probably due to implication of the great longi- 
tudinal tracts running between the brain and the cord or to dis- 
turbance of the vagus and other nuclei in the medulla. The vertigo 
is not necessarily related to the incoordination, for the latter can be 
extreme without the slightest sense of giddiness. Vertigo is probably 
a psycho-sensor}- phenomenon; whereas the incoordination is more 
intimately related to the motor apparatus. 

Titubation resembles that seen in disseminated sclerosis. The 
head is unsteady on the trunk and the unsteadiness is increased with 
every attempt at voluntary movement. This is a symptom well marked 
in clinical cases, though never so much so as the incoordination in the 
extremities. 

The attitude is often striking. I he trunl is curved, the con- 
cavity being to the side of the cerebellar lesion. The head is lateralis 
inclined to the same side and the fac< is drawn towards the shoulder. 

In experimental lesions the tendon- jerks arc exaggerated. In 
clinical cases in man they arc usually diminished or lost, though they 
may be exaggerated and long remain SO. The loss of tin knee-jerk 
occurs in irritating lesions and is probabl) due to some influence ex- 
erted upon the reflex spinal centers. Variations occur in both the 



95^ THE NON-NEURONIC DISEASES 

diminished and exaggerated types of patella disturbance from time to- 
time. 

Nystagmus is common in tumor of the cerebellum. On account 
of the intracranial pressure, ocular paralyses are not infrequent. The 
opposite sixth nerve is especially liable to suffer from pressure. This 
causes an internal strabismus in the eye on the opposite side to that 
of the cerebellar lesion. Nystagmus with ocular displacement due to- 
pressure has no special features to cause it to indicate a cerebellar 
lesion. When, however, there is no ocular displacement, or when the 
displacement is characteristic of removal of one-half of the organ, or 
when secondary pressure is not needed to explain the condition, the 
nystagmus is characteristic enough to be a valuable localizing sign. 
It is lateral. When it is spontaneous it is intensified by the voluntary 
turning of the eyes to the side of the lesion. When it is not spontane- 
ous, it may not be elicited at all or it may be observed slightly if the 
eyes are turned voluntarily away from the side of the lesion, or it may 
be very marked if the eyes are turned voluntarily to the side of the 
lesion. 

When the compression of the cerebellar lesion implicates the 
medulla, other cranial nerve symptoms may appear, such as occur in 
focal disease of the medulla : — namely, disturbed articulation, respira- 
tion and deglutition. 

A motor paresis occasionally occurs as a hemiplegia in the limbs. 
on the side of the lesion. The face remains intact. Very often the 
pyramidal tracts are compressed and there is weakness in the limbs with 
exaggeration of the tendon- jerks. 

Epileptiform convulsions are rare, but have been seen in disease 
of the cerebellum. As an indirect pressure symptom a tetanoid rigidity 
with opisthotonos has been observed. It occurs only in tumor. 

Disease of the cerebellar superior and inferior peduncles is rarely 
isolated. Rotation, forced movements, vertigo, asymmetrical displace- 
ment of the eyes are among the occasional manifestations. To these 
must usually be added signs of involvement of the pons and the fifth 
nerve. 

The cerebellum, like any other part of the brain, is subject tx> 
hemorrhage, softening, inflammation, abscess, tumor, atrophy and 
sclerosis. Occasionally it is congenitally under size and is the site of 
an agenesis. There is a cerebellar type of infantile palsy and in some 
cases of congenital atrophy the symptoms have a close resemblance to- 
those of Friedreich's disease. 

MALFORMATIONS OF THE BRA1X. 

These are of no clinical interest whatever, since they are monsters 
that never continue to live long after birth. There are many varieties, 
all of which are interesting from the embryological and developmental 
standpoint. 

Anencephaly accompanies acrania and is a condition in which, 
there is no cranial cavity or contents. The cerebellum and the primi- 
tive basal ganglia may be present in some cases. 



THE NON-NEURONIC DISEASES 957 

Micrencephaly and microcephaly means a monstrously small head 
and brain. 

Porencephaly is a partially damaged brain. I have described it 
under the head of congenital, infantile hemiplegia. 

Cyclopia is where the anterior cerebral vesicle fails to separate 
or divide and the orbits remain together with a single optic apparatus. 

Meningocele, encephalocele and hydrencephalocele are hernias, the 
nature of which is sufficientlv indicated in the names. 



SECTION D. 



GEN ERALMALADIES WITH LEADING NEURO- 
LOGICAL SYMPTOMS. 



ALCOHOLISM. 



Alcohol seems to exert a particularly deleterious influence upon 
the nervous system. Its effects are somewhat different when taken in 
large quantity occasionally from what they are when it is imbibed in 
small quantities for long periods of time. It may be studied therefore 
under the heads of acute and chronic alcoholism. In the course of 
chronic alcoholism there are occasional outbreaks of an acute condi- 
t.on, known as delirium tremens. 

Acute Alcoholism. — The ingestion of a large amount of this 
poison results in disturbances of coordination, psychosis and narcosis. 
The condition is known preeminently as drunkenness, intoxication, and 
is of physiological and toxicological interest rather than neurological. 
There is a flushed or cyanotic condition of the face, the pulse is full, 
the breathing labored. The pupils are dilated. The temperature is 
generally below normal. I nconsciousness is present, but it is not so 
dee]) but what the patient can generally be aroused momentarily with 
a great effort. Muscular twitchings, occasional convulsions and great 
stupor are not infrequently seen. This is the form of alcoholism 
usually observed in the condition known as dipsomania, wherein there 
is a strong hereditary tendency toward drink and a yielding to it by 
the indulging in a periodical spree. 

Acute alcoholism is chiefly of interest to neurology in the role it 
plays in the differential diagnosis of cerebral hemorrhage, epilepsy, 
hysteria, syncope, uraemic coma and other affections accompanied by 
unconsciousness. 

Chronic Alcoholism. — The constant drinking of alcohol and alco- 
holic beverages in amounts that never arc- sufficient to cause actual 
drunkenness produces changes of a degenerative character in nearly 
all of the tissues of the body. In a work of this sort we are only con- 
cerned with the changes that are established in the nervous tissues and 
functions. I will pass by, therefore, with the merest mention, the well- 
known alterations in the digestive apparatus, the heart and arteries, the 
kidneys and the skin. 

The earliest manifestations of chronic alcoholic intoxication are 



960 



GENERAL INTOXICATIONS 



functional in character. There is a muscular tremor which affects 
principally the lips, the tongue and the hands. It is also in the legs, but 
it is not so observable. It is an intentional tremor in part, being empha- 
sized when any voluntary movement is attempted. It causes unsteadi- 
ness and is very obvious in the speech and the writing. It is a fine yet 
irregular oscillatory tremor, and is most noticeable in the morning. 
A dose of alcohol diminishes or puts a stop entirely to it for the time 
being. 

Insomnia is a troublesome symptom in these habitues and during 
their sleep the muscles often jerk and twitch. 

The mental state is characteristic of a mild degree of degenerative 
encephalitis or meningoencephalitis. In the morning until the ac- 
customed stimulant is obtained there is dullness and apathy and some- 
times confusing headache. The temperament gradually undergoes a 
change. The individual is irritable, restless, forgetful, morally low- 
ered. He may be emotionally depressed and maudlin. He is given to 
silly sentimentalism and is often suspicious. His judgment and reason- 
ing faculties are impaired. His volition lacks force. Later on actual 
dementia may supervene. If alcohol is not a cause of dementia 
paralytica, the clinical picture it induces is very similar to it. Mental 
breakdown, epilepsy and other serious results are certainly to be at- 
tributed to it in a certain percentage of cases. 

Delirium Tremens. — This is a condition bordering on but not 
classified as an insanity. It does not follow an excessive ingestion of 
alcohol in *a person usually temperate ; it is liable to occur in a habitual 
drinker who may take an overdose of the poison. It is therefore an 
incident merely in the course of chronic alcoholism. It may even occur 
as the result of the sudden withdrawal of the poison. 

The symptoms appear gradually but rapidly, attaining their maxi- 
mum in two or three days. They may be provoked by a shock in a 
heavy drinker, a sudden fright, an accident with a profound mental 
disturbance following it. As the attack approaches the individual 
sleeps badly, has horrible dreams, is restless, depressed in spirits and 
devoid of appetite. Flashes of light appear before his eyes and noises 
of a disagreeable character ring in his ears. To overcome these he 
takes more liquor, goes to bed, and at night experiences anew the 
vivid, distressing and terrifying dreams, the visual and auditory hallu- 
cinations, the restlessness and harassing motility. As the attack draws 
on to its climax absolute insomnia occurs, the visual hallucinations 
assume definite shapes, suspicions and uneasiness are prominent and a 
veritable delirium is in evidence. 

Loquacity is enormous. The patient talks incoherently without 
cessation. He is in constant motion ; tries to get up and go out ; 
rushes toward the open window or attempts to push past his guards to 
the door. He is subject to all sorts of distressing and suspicion-pro- 
voking hallucinations. At times he trembles and cries out in evident 
alarm and fright. He declares his enemies are in the room ; that they 
are trying to injure him. He points them out, though his finger indi- 
cates only empty space. He thinks he is surrounded and overrun 
with rats and mice and snakes and other crawling vermin. This of 



GENERAL INTOXICATIONS 96 1 

course increases his terror. He is now the victim of the genuine 
"horrors." 

There is great muscular tremor and to all intents the poor fellow 
is in the state of a thoroughly terrified animal. The countenance is 
flushed and the conjunctiva congested. The pulse is soft, frequent 
and easily compressed. Perspiration is free and the temperature, 
except in mild cases, is slightly raised. The average temperature is 
about 102 or 103 degrees F. When it climbs to 108 or 109 degrees 
it is a most ominous sign. The tongue is coated heavily and there is 
absolute want of appetite. 

The insomnia continues and becomes a constant feature. In three 
or four days, if the case is favorable, the symptoms all aoate ; the rest- 
lessness subsides ; the hallucinations slowly vanish ; and the appetite 
comes back. 

In severe cases the delirium continues, and being less active is 
gradually replaced by signs of profound prostration. Stupor super- 
venes, the respirations grow shallow and the patient dies of gradual 
heart-failure. 

The symptoms caused by the polyneuritis which often constitutes 
a part of the clinical picture of chronic alcoholism will be found de- 
tailed in the section devoted to peripheral nerve lesions. 

Diagnosis. — The diagnosis of chronic alcoholism and of delirium 
tremens is not difficult. The entire condition of the patient must be 
taken into account. The cutaneous, gastric, circulatory, renal, nervous 
and mental appearances must all be given due consideration. If this 
is done it is almost impossible to make a mistake ,for scarcely any other 
disease, in fact none, presents so broad a picture. Acute mania and 
symptomatic delirium certainly do not, for they are wanting in the 
characteristic visual hallucinations and tremor. The tremor may be 
mistaken for the tremor of^dementia paralytica, but the latter is accom- 
panied by a somewhat different psychic state, more of an exaltation ana 
with more distinct delusions. The lungs should always be carefully 
examined, for in some intances an overlooked pneumonia, especially 
in a drunkard, may be the cause of the delirium starting. The same 
is to be said in regard to erysipelas and trauma. 

Pathology and Pathogenesis. — The changes observed in the 
nervous tissues in chronic alcoholism are slight and never in any 
sense characteristic. The dura may be hemorrhagic and inflamed. 
The pia-arachnoid is often opaque and thickened and chronically 
•changed. Actual signs of meningitis arc rare in either membrane. 
The underlying convolutions of the brain, in old cases, are wasted and 
depressed. Adhesions with signs of genuine meningo-encephalitis may 
be seen in some protracted eases. Berkeley, Buzzard, Hoch, Cole and 
others have found chromatolvtic and other degenerative signs in the 
neurones. Especially so in alcoholic neuritis described elsewhere. 

Though these findings, as well as others Outside of the nervous 
system, such as the congestion of the bases of the lungs, of the skin, of 
the face and of the kidneys, are highly suggestive in chronic alcohol- 
ism, they do not explain the delirium tremens. Tin- latter is patholog- 
ically as much of a mystery as ever. It is undoubtedly due to an acute 



962 GENERAL INTOXICATIONS 

process of some sort in the cerebral cortex, which disturbs the function 
of the latter, runs a definite course and then tends to subside. We 
cannot even form a guess of the nature of that process. It is more 
than a mere intoxication, such as is evidenced in the findings of simple 
chronic alcoholic poisoning. 

Prognosis. — In private practice the prognosis, for obvious rea- 
sons, is better than it is in hospital practice. Many cases recover, but 
relapses are common if the use of the poison is resumed. It is well 
for the patient to get away from his home and usual haunts ; for this 
reason institutional treatment is more favorable than home treatment. 
Complications add to the gravity of the prognosis in all cases. The 
condition of the pulse is a fair indication of the outlook. If some 
improvement is detected after sleep, a favorable temination may be 
expected. If the patient wakes up and is as bad as ever, a fatal issue is 
likely to occur soon. Very high temperature, 103 or 105 degrees, is 
an unfortunate sign. Sudden rise in temperature, with old age, are 
bad prognostics. Associated pneumonia and nephritis cloud the prog- 
nosis ; so also do traumata, wounds and operative procedures. 

Treatment. — The treatment of chronic alcoholism practically re- 
solves itself into the removal of the poison. This had better be done 
absolutely. Only in very exceptional cases will it ever be found nec- 
essary, on account of the pulse or tendency to delirium tremens, to 
allow a little alcohol or to attempt to reduce it gradually. The craving 
for the liquor should be suppressed as much as possible. Capsicum 
is effective sometimes. General tonics like strychnine, quinine, iron and 
the bitters generally are always in order. Abundant nourishing diet 
also must be prescribed, and all other measures that tend towards 
reconstruction and the health of the organism. All of this can be 
carried out best in an institution. 

The special manifestations call for no particular consideration here, 
for their management will be found described under the various dis- 
eases and disorders throughout the book. 

The delirium tremens needs careful management. The patient 
must be put under restraint and vigilantly watched night and day. 
His strength and violence is such that two male nurses will usually be 
required to handle him. No open window should be allowed and all 
dangerous articles and medicines by which he might injure himself 
should be removed. It is rarely necessary to resort to a "strait- 
jacket." Other means can sometimes be devised by which he can 
be strapped and confined to his bed. Broad straps may be attached 
to his wrists and ankles and then fastened to the sides of the bed. A 
sheet, long and strong, may be wrapped around him and the bed at the 
same time. If the hallucinations are increased by darkness or a dim 
light, the room had better be kept well illuminated. 

The alcohol should be withdrawn at once, except in those few cases 
in which there is a dangerous feebleness of the pulse. Sometimes even 
in these cases ammonia, ether, cofTee or other stimulant may be found 
available. Digitalis, at one time so much used, is now not considered 
snfe, as it accomplishes little in the mild cases and has often proved 
disastrous in the severe ones. 



GEXERAL INTOXICATIONS 9O3 

Nourishment is of supreme importance. It should be fostered as 
rapidly as possible, and in as thorough a manner as the condition of the 
organs will permit. Hence it is well to use a liquid diet for a time and 
give it every two or three hours. Beef tea, milk, lightly beaten eggs are 
available. 

The bowels should be gently and promptly moved, but severe 
purgation must be avoided. 

Ware has shown that a simple expectant treatment gives as a 
rule better results than that with medicines. However, though de- 
lirium tremens usually runs its course without being affected by medi- 
cines, a certain amount of medicinal treatment is in order. The object 
to be attained by this is the sedation of the nervous system, the produc- 
tion of sleep and the supporting of the strength. 

Bromides are usually disappointing. They may produce a certain 
amount of quietude, but they rarely cause sleep. Full doses are neces- 
sary. 

Paraldehyde was and to some extent is still popular. Bromides 
with tincture of capsicum are sometimes very effective. Chloral, unless 
markedly contra-indicated by the condition of the heart, is the most 
general available drug in this condition. Sixty grains can be given 
by the mouth and in many cases a refreshing sleep thus be secured. 
The hypodermic use of hyoscine, gr. i-ioo, or of morphine, gr. }4> 
cautiously repeated, is second in value only to chloral. Opium itself 
must be used with great circumspection. Moreover, it tends to lock 
up the secretions. Pilocarpine has been recommended, but it is dan- 
gerous to the heart. Cannabis indica has effected a desirable sedation 
in a few cases. Cold douching, cold bathing and a cold pack may be 
tried if the heart can bear the shock. A word of caution is necessary 
An the drug treatment of delirium tremens. Ofttimes in spite of the 
most heroic administration ^of hypnotics and sedatives the patient con- 
tinues wide awake. It is risky to go on plying the remedies under 
such circumstances, for as they accumulate in the system they may 
suddenly exhibit a poisonous effect and the patient die in complete 
stupor. 

THE OPIUM AND KINDRED HABITS. 

There are certain drugs which are taken medicinally at first, rarely 
as a luxury, and producing certain pleasurable or unpleasurable effects 
upon the nervous system,, are continued until the disastrous habit is 
formed. After alcohol, opium and its alkaloid morphia are most abused 
in this way. Then follows the use of chloral, cocaine, ether, chloro- 
form, paraldehyde, cannabis indica. Acute poisoning by these various 
drugs is a subject of special interest to physiology and toxicology 
more than to neurology. Chronic poisoning is pretty nearly the same, 
differing more in degree than in kind, in all of them. A description 
of chronic opium poisoning will cover more or lrss the clinical picture 
produced by all of the others. As in the- discussion of chronic alcohol- 
ism, I will briefly consider only the neurological manifestations. 

ppium Habit. — M or phino mania. Morphinism, In certain coun- 
tries where opium is used regularly there is established a partial im- 



964 GENERAL INTOXICATIONS 

munity against its deleterious effects. The effects are present, but they 
are not so obvious as they are with us. In this country the habit is 
generally started by the use of morphia to relieve pain. A headache 
or an old sciatica, the pains of chronic rheumatism or of tabes are re- 
lieved for the nonce by the drug, even upon the prescription of the 
medical attendant. When the pains return the patient acquires the 
drug for himself, learns how to use it hypodermically and so starts 
the habit. The use of chloral for insomnia, and in fact all of the 
above-named drugs, is started in this way. Women and physicians 
themselves are the leading victims of these habits. Gradually the dose 
has to be increased to obtain the desired relief, not from the pains so 
much now as from the depressing after-effects of the drug itself, so 
that ere long the patient has lapsed completely into the ranks of the 
habitues. The origin of the habit should enforce the lesson upon the 
profession to be chary in the use of these drugs, especially in chronic, 
painful states. I have seen several lives ruined by the injudicious use 
of morphine by a physician at the beginning of a simple ailment. When 
the ailment returned the patient repeated the prescription upon his own 
responsibility until he found himself in the grip of the habit. 

Symptoms. — There has never been written a more vivid account 
of the symptomatology of chronic opium poisoning than De Quincey's 
"Confessions of an Opium Eater." Every physician should be familiar 
with this masterly essay. It both teaches and warns in terms that 
cannot be mistaken. 

The symptoms at first are not at all significant and sometimes 
whole months may go by without the health showing much deteriora- 
tion. Sooner or later, however, except in the most rare instances, the 
physical and mental signs of breakdown declare themselves. These are 
subjectively noticed most as the effect of the drug wears off. There is 
a feeling of weariness, lassitude, apathy, depression and distress. 
Sometimes there is nausea and gastric discomfort. The mind is so 
depressed and the patient feels generally so bad, that he resorts to the 
drug again to get relief. As this dose wears off he experiences the 
same depression in a little more marked degree. And thus the evil 
gTows. Physically he becomes sallow in appearance, emaciated, gray 
and aged. His appetite is deranged or gone entirely. His pupils are 
dilated or unequal, except when under the direct influence of the drug. 
A general condition of asthenia and extreme physical debility ultimately 
obtains. 

Showing the degenerative effects upon the nervous system, these 
patients are immoral, irresponsible, unreliable, liars and cheats. Los- 
ing their higher psychic inhibitions, they fall a step toward the mon- 
key ; hence they are silly, cunning, without a manly sense of obliga- 
tion, selfish, maudlin and sentimental. Their mental stamina is gone 
and they lack initiative force and self-control. They are restless, 
irritable and emotional. They are sometimes the victims of most vivid 
and terrifying visual and auditory hallucinations. I once saw a pa- 
tient reach out to put her hand into the pocket of her brother, who 
she thought was standing beside the bed, but who had been dead many 
years. Itching and other paresthesias are complained of. There are 



GENERAL INTOXICATIONS 965 

occasional chills, followed by profuse sweats. Sometimes marked 
hysterical and neurasthenic symptoms dominate the clinical picture. 
Some of the profoundest neurasthenia I have ever witnessed was in 
morphine users. Unless the case is not too far gone, so that under 
heroic treatment recovery can be obtained, these patients usually go on 
increasing the dose of the drug until they become complete physical 
wrecks and mental dements, and die of inanition and heart failure. 

There is nothing to be said of the pathology of the condition. It 
is a progressive degeneration of wide extent, toxic in origin. 

The treatment is practically impossible outside of an institution. 
The patient must be isolated, systematically fed and deprived of all 
possible means of securing the drug. In mild cases the drug may be 
withdrawn abruptly and completely ; in severe cases only a gradual 
withdrawal had better be attempted. For the first week or so the 
patient had better be kept in bed and the drug gradually diminished. 
In the meantime, with the aid of baths, moral suasion, massage, etc., 
the restlessness, insomnia, nausea, vomiting and even the abdominal 
pains should be alleviated as much as possible. The bowels should 
be moved gently and regularly. The diet should be plain, nourishing 
and frequently given. It should consist of meat broths, milk, whipped 
eggs, matzoon, koumys and other light, semi-fluid articles. 

If the pulse calls for it, stimulation with aromatic spirits of am- 
monia may be given. Sleep should be fostered by warm baths, warm 
drinks and other measures ; but sometimes sulphonal, hyoscine or even 
morphia itself may have to be temporarily resorted to. 

Rapid, forced nourishment, with gradual withdrawal of the drug, 
is the sum total of the treatment in these cases. In this respect it 
follows along the same lines as that for chronic alcoholism. In spite 
of the occasional complete restoration to health, these patients too 
often lapse back into their old habit ; which makes the treatment of 
them a discouraging and thankless task. 

TETANUS. 

This is sometimes called lofkjaw. It is a most virulent form of 
infection in which there are severe tonic spasms in the muscles of the 
body. 

Etiology. — The cause of this disease is the tetanus bacillus dis- 
covered by Nicolaier and studied by Rosenbach, Kitasato and others. 
The germ enters the body through an open wound in the skin or 
mucous membrane. It is found in the earth. It has been isolated and 
cultivated. In appearance it is a slender rod which may grow into 
long threads, with one end swollen and occupied by a spore. It is an- 
aerobic, motile and develops at ordinary temperatures. The bacillus 
itself does not enter the blood or organs, but at the site of the wound 
it produces a tox-albumin, which is the most virulent form of poison 
that is known to enter the body. 

Pathology and Pathogenesis. — There are no distinctive patho- 
logical findings. The congestions observed in different parts of the 
body, the perivascular exudations and beginning chromatolytic changes 



966 GENERAL INTOXICATIONS 

in the neurones may be the result rather than the cause of the symp- 
toms. There are local manifestations, as, for instance, in and about the 
wound and the inflammation of the umbilicus in tetanus neonatorum, 
and constitutional symptoms. 

Symptoms. — We speak of a puerperal tetanus, a tetanus neona- 
torum and of endemic and epidemic attacks of the disease. Essentially 
they are all the same. 

The symptoms do not develop immediately after the invasion of 
the bacillus, but gradually. It has been suggested that this is because 
the toxin undergoes a still further change in the system. In about 
ten days the earliest signs begin to appear. The first are a little 
stiffness in the neck, slight rigidity in the jaw and difficulty in mastica- 
tion. General toxic symptoms, such as chills, fever and malaise, may 
accompany these early troubles. Gradually trismus occurs, or tonic 
contraction of the muscles of the lower jaw. This cardinal symptom 
has given the name lockjaw to the malady. As the eyebrows are ele- 
vated and the corners of the mouth are stretched laterally, the counte- 
nance assumes a horrible sort of a grimace, risus sardonicus. 

In children the symptoms remain thus in the face often, but in adults 
the musculature of the body is generally affected also. The muscles 
of the back are most frequently involved after the jaw muscles. This 
causes a bowing of the neck and back, so that the patient rests on his 
heels and occipit. So violent is this opisthotonos at times that the 
abdominal muscles have been torn directly across. If the entire body 
and limbs are rigid, the condition is known as orthotonus. A lateral 
bending of the spine causes pleurothotonos. In rare instances the ab- 
dominal muscles are so violently spasmodic that the body is curved 
forward into a condition known as emprosthotonos. Sometimes the 
chest is compressed, the glottis thrown into spasm, the respirations 
diminished and the patient almost completely asphyxiated. 

There is excruciating pain with all this violent spasm and the 
patient, silent and immovable as if clamped in a vise, is bathed in a 
profuse perspiration and reveals untold agony. The paroxysms are 
variable in duration and are easily excited. The intervals between 
the paroxysms are usually very brief. 

The temperature is usually normal, though just before death it 
may rise to no degrees F. Even higher temperatures have been seen. 
Heart-failure, asphyxia or exhaustion puts a grateful termination to 
the patient's sufferings, usually in a paroxysm. 

What is called head-tetanus is the unilateral stiffness of the jaw 
and facial muscles, from a wound on that side of the head, usually near 
the fifth nerve. 

Diagnosis. — The characteristic clinical picture and the history 
of a wound make the diagnosis of tetanus a matter of no great diffi- 
culty. The similarity between this form of toxaemia and strychnine 
poisoning is obvious. There is no history of a wound, however, in 
the latter, and trismus does not lead in the symptomatology. In tetany 
the tonic spasms begin in and are usually limited to the ends of the 
extremities, especially the fingers and hands. Doubtful cases of tetanus 



GENERAL INTOXICATIONS 



967 



can always be decided by a bacteriological examination of the secre- 
tions in the wound. 

Prognosis. — This is decidedly bad in the traumatic cases, at least 
80 per cent, dying in three or four days. In the so-called idiopathic 
cases the mortality ranges about 50 per cent. Children offer the worst 
prognosis. If the symptoms are late in coming on, if they confine them- 
selves to the jaw and face, and if there is little or no fever, hope of 
recovery may be entertained. 

Treatment. — Strict attention to the wound is the first requisite. 
It should be thoroughly excised, antiseptically washed and according 
to Tizzoni treated with nitrate of silver to destroy the germ in situ. 

A dark and perfectly still room should be the domicile of the pa- 
tient. Extraordinary care should be exercised to avoid every possible 
sort of irritation. Noise, light, drafts of air, change of nurses should 

FIGURE 211. 




Tetanus. (After Sir Charles Bell.) 

be guarded against. Even such strenuous efforts will not forestall the 
paroxysms in most cases. 

Feeding is a problem on account of the locked condition of the 
jaws. A tube may be passed through the nostrils into the gullet or 
into the rectum and liquid diet administered in that way. 

The control of the spasms is best secured with full doses of mor- 
phia. Chloroform inhalations and such drugs as the bromides, chloral, 
cannabis indica, calabar bean, curare are available agents. Recovery 
has sometimes followed their employment. 

Blood-scrum therapy seems to hold out some hopes in this disease. 
By Tizzoni and Cantani the blood-serum of immunized animals has 
been used with some degree of success. Behring and Roux haw each 
prepared an antitoxine serum. That of Tizzoni seems to be the most 
successful. It is recommended that j.j^ grammes of the Tizzoni anti- 
toxine be employed for the first dose and 0.6 grammes for subsequent 
doses. 

From the observations of Marie and Morax, of Meyer and Ransom 



968 GENERAL INTOXICATIONS 

and of Rogers, it would seem to be advisable to expose the nerves of 
the part in which the primary infection lies as near the cord as possible 
and to inject directly into the substance of each nerve the antitoxine. 
This prevents the absorption of more poison from the wound. An 
injection should then be made low down in the spinal cord or in several 
places. The injection may be made as in an ordinary lumbar puncture. 

HYDROPHOBIA. 

This is sometimes called lyssa and rabies. It is an acute disease 
of warm-blooded animals ; is dependent upon a specific virus ; and is 
characterized by marked nervous symptoms. 

Etiology. — The poison that causes rabies is found chiefly in the 
nervous system and in some secretions such as the saliva. We know 
nothing of its essential nature. Many animals are susceptible to it, 
namely, man, the dog, the wolf, the cat and by inoculation the ox, 
horse, pig and skunk. 

The period of incubation is shorter in children than it is in adults. 
Bites are more dangerous in exposed parts of the body, like the face 
and hands, than they are in covered parts like the trunk and legs. 
Large, punctured wounds afford the most ready entrance to the poison. 
According to Horsley, only 15 per cent, of those bitten by dogs be- 
come affected with the disease. Wolf bites give a higher percentage. 

The incubation period in man ranges from two weeks to three 
months. The average time is about six or, eight weeks. 

Pathology and Pathogenesis. — The blood vessels of the cere- 
brospinal nervous system are congested, particularly in the medulla. 
There is an exudation of leucocytes in the perivascular spaces and 
minute hemorrhagic extravasations. The virus is found abundantly 
in the brain, spinal cord and nerves, but not in the kidneys, spleen or 
liver. Congestions are observed in the stomach, larynx, trachea and 
bronchi. 

Symptoms. — These appear after a variable interval after the in- 
oculation. For the sake of practical convenience, they are divided 
into those of the premonitory, excitable and paralytic stages. 

The earliest signs of the malady are irritability, restlessness, mental 
depression, fear of impending trouble, pain and numbness near the 
bite, headache, loss of appetite and insomnia. Often there is a general 
hyperesthesia to all forms of sensation. Light and noise irritate the 
patient. The larynx being congested, the voice grows husky and 
deglutition becomes embarrassed. The pulse is somewhat rapid and 
the temperature is slightly elevated. 

Gradually the hyperesthesia increases, the restlessness grows 
worse, the dejection passes into alarm and general spasms begin to 
develop. This is the beginning of the stage of excitement. As this 
advances, every sort of external stimulation, a noise, a bright light, a 
mere verbal suggestion, a draught of air may provoke a most violent 
spasm. The spasms are strikingly in the areas supplied by nerves from 
the medulla, namely, the muscles of the larynx and mouth. They 
are reflex spasms and are exceedingly painful. An attempt to drink 



GENERAL INTOXICATIONS 969 

water sets up the spasm so violently that the patient dreads the very 
thought of drinking, hence the name of the malady, hydrophobia. 

The mind is usually affected along with this spasmodic condition. 
The patient is maniacal, though between the spasms he may be calm 
and rational. He is usually harmless and even takes care not to hurt 
any one unless his mania is furious. The temperature is generally ele- 
vated in this stage. 

After a few days the paralytic stage comes on, terminating in 
coma and death in a few hours. Heart failure and syncope close the 
distressing scene. 

Pseudo-hydrophobia or lyssophobia is in all probability a hysteroid 
trouble, developed upon a background of fear and dread. An indi- 
vidual who has been bitten may undergo and simulate all the phenome- 
na of true rabies in a mild degree. The condition lasts longer than in 
the genuine disease and the patient always recovers. 

Diagnosis. — This is easy in view of the history of a bite and the 
characteristic symptomatology. In cases of doubt, or better still, in 
all cases, so as even to forestall any possible doubt, the animal that 
has bitten the patient should be made to furnish inoculations from the 
region of the medulla. If these be tested upon other animals, especially 
the rabbit, the paralytic form of the disease will appear in from fifteen 
to twenty days. This will tell us what to expect in the patient and 
confirm the diagnosis. 

Treatment. — This is not the place to discuss the general prophy- 
laxis of hydrophobia and the laws that should be passed in regard to 
the muzzling of dogs. The preventive inoculations of Pasteur do cer- 
tainly seem to be effective in man, if we are to judge from the sta- 
tistics sent out by the various Pasteur Institutes throughout the 
world, and especially by the one in Paris. 

The management of a case of hydrophobia is a most unsatisfactory 
task. There is no specific remedy and so the treatment must perforce 
be entirely symptomatic. It must also be heroic. The wound, of 
course, should be antiseptically washed, cauterized and kept open for 
several weeks. 

When the disease has developed it is absolutely incurable. Chloro- 
form and morphia are about the only agents at our command to assist 
in alleviating the patient's sufferings. Chloral, bromides, hyoscine 
are practically useless. Cocaine may be painted on the throat, enabling 
the patient to swallow somewhat. Rectal nutrient enemata as a rule, 
however, will have to be resorted to. 

Arthritis Deformans. — I nder this name are probably masking 
a number of conditions, so that we arc only justified in regarding the 
term as merely representing a symptom-complex. The view is gaining 
ground that an infection or toxemia underlies the manifestations. The 
microbic origin of the disease is not satisfactorily established yet, 
though Schuller, Bannatyne and Blaxall and others have found micro- 
organisms in the fluids of the joints. The affection IS often associated 
with previous infections, as shown by the Statistics of Stewart and 
others. This local infection theory i> accepted by Baumler, but not by 
Osier and others. 



97o 



GENERAL INTOXICATIONS 






An attempt is being made, and I think somewhat successfully, to 
bring the old neurotic theory of the origin of arthritis deformans in 
line with the infection or toxemic theory. There can be no doubt 



FIGURE 212. 





Arthritis deformans. (From a photograph in the Pathological Museum of 
the Med. Depart, of the University of Illinois.) 

of the tropho-neurotic nature of the malady in some of its phases at 
least. We are familiar with the acute and chronic forms of arthritis 
that often accompany gross disease of the cord. The arthropathies of 



GENERAL INTOXICATIONS 9/ E 

tabes are among the latter's cardinal symptoms. In dementia para- 
lytica, syringomyelia, hemiplegic conditions and diseases of the 
peripheral nerves, atrophy and other changes not infrequently occur in 
the bones and in and about the joints. Hence the dependence of 
trophic joint troubles upon disease of the central nervous system can- 
not be gainsaid. 

There are several features in rheumatoid arthritis that suggest 
most forcibly a central nervous explanation of the trouble. The 
changes in the joints are all but identical with those that occur in the 
spinal arthropathies just mentioned. Similar changes of a trophic 
nature occur in various tissues in arthritis deformans, just as they do 
in many spinal diseases. The skin becomes glossy, the nails get brittle, 
the bones and muscles undergo dystrophic alterations. The muscles 
sometimes markedly atrophy. The distribution of the joint and other 
changes is symmetrical, thus suggesting a central cause for them. 
And finally neuritis is often found clinically and pathologically in the 
disease. Osier notes that in a case of chronic arthritis from Dejerine's 
service, Triboulet and Thomas found upon post mortem a sclerotic 
condition of the posterior columns of the cord. Puerperal infection 
seems to have been the primary cause of the trouble. 

Llewelyn Jones has recently called attention to the relationship 
of rheumatoid arthritis to some other neurotic affections, particularly 
tetany, Raynaud's disease and exophthalmic goitre. In all of these 
troubles there is more or less similarity in the vasomotor phenomena, 
the muscular cramps and the periarthritic swellings. As Jones sug- 
gests, these diseases may all pass insensibly into each other as members 
of one family group, owning one common parent origin, a cerebro- 
spinal toxcemia. Macalister has adopted views similar to those of 
Jones. &• 

Upon these and other grounds, I am inclined to regard arthritis 
deformans as a cerebro-spinal tropho-neurosis, dependent upon some 
obscure form of toxaemia. I have not classified the malady among the 
tropho-neuroses in the earlier part of the volume, because there are 
needed more data, especially from examination of the central nervous 
system, to positively affirm that the disease is solely of neurotic origin. 

Other Toxemic Troubles. — There are many other neurotic mani- 
festations and symptom-complexes that are not sufficiently sui generis 
to warrant giving them the dignity of a special nosological position 
among nervous diseases. Such, for instance are the nervous types of 
influenza, with their severe headache, profound prostration, pains in 
the back and joints, depression of spirits, melancholia and even de- 
mentia; pertussis, with its spasmodic Spells; and many cutaneous ex- 
hibitions, such as urticaria, herpes, pruritis and other paresthesia. 
Most of these symptom-groups can be referred to neuritis, poliomyelitic 
processes, disease of the posterior rool ganglia and other disorders nf 
the lower or peripheral neurones. 



Finis. 



GENERAL INDEX. 



Abdomen, scaphoid, 803 
Abiotrophy, 352 
Aboulia, 106 
Abscess, cerebellar, 871 

pontile, 871 

bulbar, 871 

of the spinal cord, 555 

cerebral, 867 
Abnormal emotional states, 759 

intellectual states, 756 
Accommodation reflex, 63 
Acoustic striae, 704 
Acquired diseases, 100 
Acromegaly, 339 
Acute delirium, 874 

ascending paralysis, 431 
Acroparesthesia, 316 
Actinomycosis, 910 
Acrania, 956 
Adiposis dolorosa, 345 
^sthesiometer, 49 
Afferent diseases, 367 

path, 98 
Ageusia, 658 
Agenesis, general, 422 
Agitans, paralysis, 299 
Agraphia, 767, 769 
Age in etiology, 30 
Agoraphobia, 163 
Ainhum, 350 
Akinesia algera, in 
Akinesis, 51 
Akatama, 590, 603 
Alopecia, 170 
Allorhythmia, 169 
Alcoholism, 959 
Alcoholic coma, 761 

polyneuritis, 592 
Allocheiria, 48 

Alternate hemiplegia, yyy, 924 
Alternating anaesthesia, 954 
Alexia, 762, 767, 770 
Amblyopia, 787 
Ambiguous layer. 683 
Amyelinic neuroma, 609 
Amimia, 771 



Amnesia, 595, 762 

Amnesic aphasia, 767, 769 

Amyelia, 570 

Amnestic aphasia, 769 

Amyotrophic lateral sclerosis, 395, 401 

Amaurotic family idiocy, 451 

Anterior fundamental root zone, 476 

radicular zone, 475 

fossa, tumor of. 925 

poliomyelitis, acute, 541 * 

commissure, 472 
Antero-lateral tract, 476, 484 
Anode, 65 
Aphasia, 762, 767 

sensory, 769 

pressure. 771 

visual, 770 

amnestic, 769 ' 

tactile, 771 
Aphonia, 766 

hysterical, 124 
Apoplexy, hemorrhagic, 828 

ingravescent, 837 

spinal, 529 
Apoplectiform bulbar paralysis, 952 
Apoplexia parva, 188 
Apoplexie foudroyante, 830 
Apoplectic coma. 762 
Apparatus, nervous, 97 
Area, auditory, 722 

olfactory, 722 
Analgesia, 48 
Analgesic paralysis, (>23 
Anaesthesia, 47 

crossed, 779, 954 
Anaesthetic leprosy, 568 
Angular curvature. 501 
Angioneurotic oedema, 318 
Aneurism, intracranial, 934 
Animal, a vertebrate. 459, 
Ankle clonus, 6l 

reflex, 6i 

Aneurisms, miliary. 826 

Aneurismal erosion of vertebrae, s^x; 
Anaemia, spinal, 52; 

cerebral, Xjj 

hydrocephaK -id, « w -'4 



974 



GENERAL INDEX 



Anosmia, 779 
Anencephaly, 956 
Angioneuroses, 306 
Anarthria, 766 
Anidrosis, 74 
Area, gustatory, 722 

visual, 722 
Areas, motor, 723 

sensorial, 719 
Argentic polyneuritis, 598 
Arthropathy, 383 
Arthritic palsy, 617 
Arteriosclerosis, 828 
Arterial system, cortical, 711 

ganglionic, 713 

choroidal, 714 
Arteritis, degenerative, 829 

syphilitic, 881 
Arthritis deformans, 969 

of spine, 510 
Arteriae sulci, 465 
Articular hydrops, 2> 22 ~ 
Articulate animal, an, 459 
Argyria, 598 
Arthralgia, 596 
Arrhythmia, 169 
Arachnoid, 462, 667 
Arachnoidal granulations, 667 
Arborization, 91 
Arm palsy, lower, 616 

upper, 616 
Argyll-Robertson pupil, 63, 376 
Architecture, neuronic, 95 
Arbor vitae, 707 
Arsenical polyneuritis, 597 
Ascending current, 85 

neuritis, 582 
Asterion, 679 
Astereognosis, 48 
Astasia abasia, 107 
Association centers, 747 

tracts, 472, 735 
Associated movement, 52, 776 
Astrophobia, 163 
Asphyxia, local, 310 
Aspiration pneumonia, 660 
Asymmetrical cord, 570 
Atavism, 28 
Ataxia, 377, 48, 54, 779 

hereditary, 444 

cerebellar, 444, 447 

of thought, 449 

locomotor, 367 
Ataxic paraplegia, 439 

aphasia, 767, 768 

hemiplegia, 836 



Atrophy, 74 

deuteropathic, 393 

optic, 784, 787 

lipomatous muscular, 416 

occupation muscular, 430 

progressive muscular, 392 

protopathic, 393 
Atrophic spinal paralysis, 541 
Attitude, 45 
Atelomyelia, 570 
Atheroma, arterial, 828 
Athyrea, 334 . 
Athetosis, 53, 425, J77, 778 
Aurium, tinnitus, 166 
Aura, 198 
Auditory symptoms, 792 

area, 722 
Aural vertigo, 153 
Automatic reflex action, 476 
Automatism, 142 
Autohypnosis, 145 
Axis — cylinder, 91 

B 

Babinski reflex, 56 
Baths, 79 

Basedow's disease, 322 
Baillarger, line of, 683 
Basilar meningitis, 814 
Bechterew, striae of, 683 
Betz, giant cells of, 685 
Bell's mania, 874 

palsy, 653 
Beriberi, 590, 603 
Biot's respiration, 753 
Bifida, spina, 569 
Bladder crises, 382 
Blepharospasm, 167 
Blindness, word, 762, 770 

psychic, 791 
Blushing, 167 
Blind spot, 781 
Body, pineal, 739 

pituitary, 739 
Bodies, olivary, 705 

Pacchionian, 667 
Borborygmi, 168 
Brain, diseases of, 662 

anatomy, 662, 668 

diseases, symptoms of, 662 

weight of, 664 

microcephalic, 664 

megalocephalic, 664 

membranes of, 665 

conducting tracts of, 710, 735 

circulation of, 710 



GENERAL INDEX 



975 



symptoms of disease of, 749 

localization symptoms, 750 

general symptoms, 751 

tumor of, 909 

tumor of the base of, 925 

vesicles, 668 

membranes, diseases of, 793 

circulatory diseases of, 821 

the, 460, 663, 714 

veins of, 714 

malformations of, 956 

sand, 696 

structure, 680 
Bregma, 679 
Broca's center, 724 
Brown-Sequard syndrome, 492, 530 
Brachypncea, 382 
Brachial plexus, 614 
Bradycardia, 169 
Bulbar paralysis, apoplectiform, 952 

paralysis, hereditary, 953 

paralysis, progressive, 395, 406, 951 

abscess, 871 
Burdach's column, 475, 484 
Bursitis, 633 



Capsule, internal and external, 689 

internal, functions, 736 
Cannabis indica habit, 963 
Caisson disease, 570 
Cauda equina, diseases of, 573 
Case-book chart, 44 
Caries of the vertebrae, 499 
Catalepsy, 146 
Calcaneus, pes, 548 
Cajal, cells of, 685 
Cardiac crises, 382 
Cavities of spinal cord, 562 
Cathode, 65 

Canals, semicircular, 149 
Carcinoma of the brain, 910 
Caudate nucleus, 690 
Cauda equina, 463 

tumor of, 557, 559 
Causalgia, 48 

Cerebro-spinal meningitis, epidemic, 808 
Cerebral anaemia, 822 

hyperaemia, 825 

hemorrhage, 828 

embolism, 845 

thrombosis, 845 

palsy of childhood, 854 

diplegia, 854 

paraplegia, 854 

abscess, 867 



Cerebral — 

syphilis, 877 

localization, 662, 714 

cortex, 672, 681, 717 

concussion coma, 761 

epiphysis, 695 
Cerebro-spinal fluid, 495 
Cerebellar agenesis, 450 

cortex, 707 

abscess, 871 

tract, direct, 475. 484 
Cerebellum, 705, 740 

tumor of, 922 

diseases of, 954 
Center, Broca's. 724 
Centers, cortical, 717 

spinal, 480 

association, higher, 747 

psychomotor, 729 
Central convolutions, tumor of, 920 

myelitis, 537 

scotoma, 787 

ganglia, tumor of, 921 
Cells of Purkinje, 707 
Cervico-brachial neuralgia, 251 
Cervical enlargement, 463 

opisthotonos of infants, 820 

myelitis, 536 

hypertrophic pachymeningitis, 514 
Cephalic flexures, 670 
Cephalaea, 234 
Cephalalgia, 234 
Chemosis, 811 
Choked disc, 784 
Choroidal arterial system, 714 
Chloroform habit, 963 
Chromophyllic substance, 93 
Cheyne-Stokes respiration, 753 
Chromatolysis, ^6 
Chorea, 286 

habit, 265 

procursive, 299 

magna, 132, 299 

corpuscles, 289 

festinans, 299 

hysterical, 132, 299 
Chronic chorea. 297 

infantile meningitis, 820 

meningitis, 820 
Chiasm, optic. 694, 788 
Cholesteatoma of the brain. 910 
Chorda tympani, 701 
Chloral hal.it. 963 
( livostek's sign, 260 
Ci net nrc pain, 535 
Ciliary body, 707 



974 



GENERAL INDEX 



Anosmia, 779 
Anencephaly, 956 
Angioneuroses, 306 
Anarthria, 766 
Anidrosis, 74 
Area, gustatory, 722 

visual, 722 
Areas, motor, 723 

sensorial, 719 
Argentic polyneuritis, 598 
Arthropathy, 383 
Arthritic palsy, 617 
Arteriosclerosis, 828 
Arterial system, cortical, 711 

ganglionic, 713 

choroidal, 714 
Arteritis, degenerative, 829 

syphilitic, 881 
Arthritis deformans, 969 

of spine, 510 
Arteriae sulci, 465 
Articular hydrops, 322- 
Articulate animal, an, 459 
Argyria, 598 
Arthralgia, 596 
Arrhythmia, 169 
Arachnoid, 462, 667 
Arachnoidal granulations, 667 
Arborization, 91 
Arm palsy, lower, 616 

upper, 616 
Argyll-Robertson pupil, 63, 376 
Architecture, neuronic, g5 
Arbor vitae, 707 
Arsenical polyneuritis, 597 
Ascending current, 85 

neuritis, 582 
Asterion, 679 
Astereognosis, 48 
Astasia abasia, 107 
Association centers, 747 

tracts, 472, 735 
Associated movement, 52, 776 
Astrophobia, 163 
Asphyxia, local, 310 
Aspiration pneumonia; 660 
Asymmetrical cord, 570 
Atavism, 28 
Ataxia, 377, 48, 54, 779 

hereditary, 444 

cerebellar, 444, 447 

of thought, 449 

locomotor, 367 
Ataxic paraplegia, 439 

aphasia, 767, 768 

hemiplegia, 836 



Atrophy, 74 

deuteropathic, 393 

optic, 784, 787 

lipomatous muscular, 416 

occupation muscular, 430 

progressive muscular, 392 

protopathic, 393 
Atrophic spinal paralysis, 541 
Attitude, 45 
Atelomyelia, 570 
Atheroma, arterial, 828 
Athyrea, 334 . 
Athetosis, 53, 425, 777, 778 
Aurium, tinnitus, 166 
Aura, 198 
Auditory symptoms, 792 

area, 722 
Aural vertigo, 153 
Automatic reflex action, 476 
Automatism, 142 
Autohypnosis, 145 
Axis — cylinder, 91 

B 

Babinski reflex, 56 
Baths, 79 

Basedow's disease, 322 
Baillarger, line of, 683 
Basilar meningitis, 814 
Bechterew, striae of, 683 
Betz, giant cells of, 685 
Bell's mania, 874 

palsy, 653 
Beriberi, 590, 603 
Biot's respiration, 753 
Bifida, spina, 569 
Bladder crises, 382 
Blepharospasm, 167 
Blindness, word, 762, 770 

psychic, 791 
Blushing, 167 
Blind spot, 781 
Body, pineal, 739 

pituitary, 739 
Bodies, olivary, 705 

Pacchionian, 667 
Borborygmi, 168 
Brain, diseases of, 662 

anatomy, 662, 668 

diseases, symptoms of, 662 

weight of, 664 

microcephalic, 664 

megalocephalic, 664 

membranes of, 665 

conducting tracts of, 710, 735 

circulation of, 710 



GENERAL INDEX 



975 



symptoms of disease of, 749 

localization symptoms, 750 

general symptoms, 751 

tumor of, 909 

tumor of the base of, 925 

vesicles, 668 

membranes, diseases of, 793 

circulatory diseases of, 821 

the, 460, 663, 714 

veins of, 714 

malformations of, 956 

sand, 696 

structure, 680 
Bregma, 679 
Broca's center, 724 
Brown-Sequard syndrome, 492, 530 
Brachypncea, 382 
Brachial plexus, 614 
Bradycardia, 169 
Bulbar paralysis, apoplectiform, 952 

paralysis, hereditary, 953 

paralysis, progressive, 395, 406, 951 

abscess, 871 
Burdach's column, 475, 484 
Bursitis, 633 



Capsule, internal and external, 689 

internal, functions, 736 
Cannabis indica habit. 963 
Caisson disease, 570 
Cauda equina, diseases of, 573 
Case-book chart, 44 
Caries of the vertebrae, 499 
Catalepsy, 146 
Calcaneus, pes, 548 
Cajal, cells of, 685 
Cardiac crises, 382 
Cavities of spinal cord, 562 
Cathode, 65 

Canals, semicircular, 149 
Carcinoma of the brain, 910 
Caudate nucleus, 690 
Cauda equina, 463 

tumor of, 557, 559 
Causalgia, 48 

Cerebro-spinal meningitis, epidemic, 808 
Cerebral anaemia, 822 

hyperaemia, 825 

hemorrhage, 828 

embolism, 845 

thrombosis, 845 

palsy of childhood, 854 

diplegia, 854 

paraplegia, 854 

abscess, 867 



Cerebral — 

syphilis, 877 

localization, 662, 714 

cortex, 672, 681, 717 

concussion coma, 761 

epiphysis, 695 
Cerebro-spinal fluid, 495 
Cerebellar agenesis, 450 

cortex, 707 

abscess, 871 

tract, direct, 475. 484 
Cerebellum, 705, 740 

tumor of, 922 

diseases of, 954 
Center, Broca's, 724 
Centers, cortical, 717 

spinal, 480 

association, higher, 747 

psychomotor, 729 
Central convolutions, tumor of, 920 

myelitis, 537 

scotoma, 787 

ganglia, tumor of, 921 
Cells of Purkinje, 707 
Cervico-brachial neuralgia, 251 
Cervical enlargement, 463 

opisthotonos of infants, 820 

myelitis, 536 

hypertrophic pachymeningitis, 514 
Cephalic flexures, 670 
Cephalaea, 234 
Cephalalgia, 234 
Chemosis, 811 
Choked disc, 784 
Choroidal arterial system, 714 
Chloroform habit, 963 
Chromophyllic substance, 93 
Cheyne-Stokes respiration, 753 
Chromatolysis, 36 
Chorea, 286 

habit, 265 

procursive, 299 

magna, 132, 299 

corpuscles, jtt; 

festinans, 299 

hysterical, 132, 299 
Chronic chorea, 297 

infantile meningitis, 820 

meningitis, Sao 
Chiasm, optic, 694, 788 
Cholesteatoma of tin- brain. 910 
Chorda tympani, 701 
Chloral habit. 963 
Chvosu-k\ sign, 
Cincture pain. 535 
Ciliary body, 707 



976 



GENERAL INDEX 



Circle of Willis, 711 
Circulation of the brain, 710 
Circulatory diseases of brain, 821 
Claustrum, 689 

Clarke's vesicular column, 469 
Clonus, ankle, 61 

jaw, 62 
Clonic spasm, 52 
Climate in etiology, 32 
Climato-therapy, 87 
Classification of diseases, 22 
Claustrophobia, 163 
Clavus, 109 
Cocaine habit, 963 
Coccydynia, 251 
Conarium, 695 
Collateral, 91 
Colonies, epileptic, 215 
Coccygeal neuralgia, 251 
Conus medullaris, 463 
Cornual myelitis, 541 
Cord, the, 460 

tumor of, 555 

abscess of, 555 

malformations of, 569 

spinal, diseases of, 526 

spinal, anatomy, etc., 459 
Cortex, cerebellar, 707 

cerebral, 672, 681, 717 
Cortical layers 684 

arterial system, 711 

deafness, 723 
Corticopetal path, yz2> 
Conjugate deviation, 777 
Conducting tracts of the brain, 710 
Compression paralysis, 619 

myelitis, 537 
Compressed air paralysis, 570 
Corpus callosum, tumor of, 922 
Corpus dentatum, 707 
Consciousness, 748 

loss of, 760 

double, 762 
Concussion, spinal, 574 
Congenital myotonia, 284 
Conduction, spinal, 476, 481 
Convulsion, 52, 772 
Convolutions, cerebral, 672 
Corticofugal path, 733 
Coma, 761 

Communicantes, rami, 308 
Comma tract, descending, 475 
Commissure, gray, 460 

anterior, 472 
Contraction of visual field, 780 
Contracture, 53, 776 



Confabulation, 595 
Coprolalia, 270 
Corpus callosum, 736 
Corpora geniculata, 692, 738 

subthalamica, 692, 695, 738 

albicantia, 692, 739 

quadrigemina, 692, 695, 738 

striata, 689, 737 

quadrigemina, tumor of, 922 
Coxitis, 550 
Coxalgia, 633 
Cramp, 52, 167 

writer's, 273 
Cranial nerves, diseases of, 643 

nerve nuclei, 698 
Cranio-cerebral topography, 677 
Craft palsy, 430 

paralysis, 581, 621 
Cretinism, 334, 337 
Cremasteric reflex, 56 
Crossed pyramidal tracts, 472, 483 

paralysis, 655 

paralysis, 924 

paralysis, 51 

anaesthesia, 779, 954 
Cross-legged progression, 424 
Crises, 381 

Cry, hydrocephalic, 817 
Crutch palsy, 581, 620 
Crura cerebri, 739 
Curvature, angular, 501 

lateral, 509 
Cup, physiological, 784 
Cyclopia, 957 
Cytoplasm, 93 

Cysticercus of the brain, 910 
Cyrtometer, 678 

D 
Deafness, hysterical, 124 

cortical, 723, 762 

word, 723, 762, 769 
Deep reflexes, 57 
Deformans, arthritis, 969 

osteitis, 343 
Delirium, 760 

hallucinatory, 107 

acute, 874 

grave, 874 

tremens, 960 
Dentate body, 707 

nucleus, 739 
Depression, 760 
Deuteropathic atrophy, 393 
Degeneration, 36, 584 

reaction of, 170 

primary, 580 



GENERAL INDEX 



977 



Degeneration, secondary, 458, 580 
Descending current, 85 

comma tract, 475 
Demarche tabeto-cerebelleuse, 448 
Degeneracy, 29 
Decentralization, 36 
Dercum's disease, 345 
Dentate ligament, 462 
Deviation, conjugate, yyy 
Delusion, 758 
Dendrite, 91 

Dementia paralytica, 888 
Dermographia, 74 
Diatheses in etiology, 33 
Diagnosis, general, 41 
Diabetic polyneuritis, 603 
Digiti mortui, 311 
Dietetics, 78 
Dipsomania, 959 
Direct pyramidal tracts, 472 
Diplegia, 774 

cerebral, 854 
Diplegic facial palsy, 654 
Diseases, neuronic, 89 

primary, 20 

secondary, 21, 458 
Disorientation, 595 
Disseminated sclerosis, 901 

nodal neuritis, 584 

myelitis, 537 
Dislocations of vertebrae, 496 
Disc, choked, 784 
Diplomyelia, 570 
Diphtheritic polyneuritis, 599 
Direct cerebellar tract, 475, 484 
Diencephalon, 668 
Diastematomyelia, 570 
Diaphragmatic paralysis, 613 
Diaphragm sellae, 666 
Diplopia, 647, 792 
Diuresis, 74 
Diver's paralysis, 570 
Doctrine, the neurone, 89 
Dolorosa, adiposis, 345 

puncta, 629 

tubercula, 611 
Double consciousness, 762 
Dorsal nerves, 624 

myelitis, 536 
Dolorous paraplegia, 508 
Dorsalis, tabes, 367 
Dreaming, 141 
Dropsy, sleeping, 148 
Drunkard's paralysis, 581 
Dura mater, 461, 665 
Dysthyroidation, 323 



Dysarthria, 407, j66 

Dystrophy, progressive muscular, 409 

Dyskinesis, 53 

Dysphagia, 658 

Dyspepsia, nervous, 168 

Dynamometer, 52 



Echinococcus of the brain, 910 
Echolalia, 270 
Echokinesis, 270 
Eclampsia, 252 

infantum, 252 

parturientium, 254 

ursemica, 255 
Efferent diseases, 392 

path, 98 
Efferentes, rami, 308 
Electric chorea, 299 
Electro-diagnosis, 64 

therapy, 85 
Elephantiasis mollis, 610 
Embolism, spinal, 528 

cerebral, 845 
Emissive centers, 717 
Emission, seminal, 170 
Emprosthotonos, 966 
Emotional states, abnormal, 759 
Encephalomalacia, 845 
Encephalometer, 678 
Encephalitis, 864 

hemorrhagic, 865 

suppurative, 867 
Encephalocele, 957 , 

Encephalon, 663 
Encephalopathia saturnina, 596 
Endoneurium, 577 
Endogenous diseases, 25 
Endemic polyneuritis, 603 
Endarteritis, spinal, 528 
Enlargement, cervical and lumbar, 463 
Epineurium, $jj 
Epilepsy, [88 

hystero, 120 

Jacksonian, 206 

symptomatic, 206 

traumatic, 190 

reflex, 191 

senile, 191 
Epileptic fit, 200 

coma, j()\ 

face, 209 

colonies, 215 
Epileptic equivalent, 205 
Epilepticus, status, 189, 
Epiphysis cerebri. 695, 739 



97 8 



GENERAL INDEX 



Epidemic cerebrospinal meningitis, 808 

Equivalent, epileptic, 205 

Equivalents, hemicranial, 230 

Equi no- varus. 548 

Erythromelalgia, 314 

Erigentes, nervi, 308 

Erosion of vertebrae, aneurismal, 509 

Erythrophobia, 167 

Erb's sign in tetany, 260 

palsy, 616 

spinal paralysis, 523 
Essential contracture, 256 
Etiology, general, 25 
Ether habit, 963 
Examination of patient, 41 
Excitation, reaction of, 260 
Exaltation, 759 
Exudative, inflammation, 39 
Exogenous diseases, 25 
Exercise, physical, 79 
External pachymeningitis, 512 
Exophthalmos, 324 
Exophthalmic goitre, 322 



Facts, 184 

Facies epileptica, 209 

Facial hemiatrophy, 348 

tic, 265 
Factitia, urticaria, 168 
Failure, mental, 762 
Familial diseases, 29 
Falling sickness, 188 
Fasciculus, solitary, 704 
Fear neuroses, 163 
Fetichism, 170 
Fever, spotted, 808 
Fibroma molluscum multiplex, 609 
Fissures, cerebral, 672 
Fibres, tangential, 683 
Fibrillary tremor, 53 
Fibroma of the brain, 910 
Fit, epileptic, 200 
Filum terminale, 461, 463 

diseases of, 573 
Flaccid paralysis, 51 
Fluid, cerebro-spinal, 495 
Flexures, cephalic, 670 
Forced movement, 53 
Focal neuritis, 629 
Frankel's exercises, 391 
Folie musculaire, 291 
Folie de grandeur, 894 
Frontal lobes, tumor of, 918 
Friedreich's disease, 444 
Fractures of the vertebrae, 496 



Frontal lobes, functions of, 719 
Functional diseases, 40 
Funiculus, 577 

gracilis, 475 

cuneatus, 475 



Gal<eni, venae, 714 
Ganglia, auditory, 698 

Gasserian, 698 

jugular, 658, 698 

geniculate, 698 

petrous, 658, 698 
Ganglionic arterial system, 713 
Ganglion habenulae, 691, 696 
Gastric crises, 381 
Gait, 45 

hemiplegic, 834 
Gangrene, symmetrical, 310 
Gelatinous substance of Rolando, 469 
General paresis, 888 
Genius, 29 
Gesture aphasia, 767 
General tic, 269 

Gilles de la Tourette's disease, 269 
Gland, pineal, 695, 739 
Globus hystericus, 119 

pallidus, 690 
Glomerulus, olfactory, 688 
Glabella, 679 
Glioma of the cord, 568 

of the brain, 910 
Gliosis, 40, 457, 563 
Gliomatosis, 40 
Glossodynia, 250 
Giant swelling, 318 

cells of Betz, 685 
Gigantism, 343 
Girdle pain, 535 
Goitre, exophthalmic, 322 
Goll's column, 475, 484 
Gowers' tract, 476, 484 
Grand mal, 188, 200 
Gray matter, 97 

commisure, 460 
Giant urticaria, 320 
Granulationes arachnoideales, 667 
Granular meningitis, 815 
Grave's disease, 322 
Grave, delirium, 874 
Gratiolet, radiations of, 694 
Graphospasm, 273 
Grandeur, folie de, 894 
Gustatory symptoms, 792 

area, 722 



GENERAL INDEX 



979 



Gummatous meningitis, 878 

neuritis, 521 

meningitis, 521 
Gymnastics, 83 
Gyri, cerebral, 676 

H 

Habenulae, ganglion, 691, 696 

Habit chorea, 265 

Haematoma, 794 

Hemoglobinuria, 312 

Haemic headache, 235 , 

Hallucinatory delirium, 107 

Hallucination, 757 

Hand, preacher's, 515 

Head-tetanus, 966 

Headache, 234, 751 

paroxysmal, 226 
Heart, tobacco, 169 
Hematomyelia, 528 
Hematorrhachis, 524 
Hematomyeloporosis, 529 
Hemicranicus, status, 230 
Hemiachromatopsia, 789 
Hemiageusia, 655 
Hemichorea, 776 
Hemiatrophy, facial, 348 
Hemianopsia, 782, 789 
Hemicranial equivalents, 230 
Hemiplegia, 51, 724, 773 

progressive, 885 

infantile, 854 

alternate, yyy, 924 

ataxic, 836 
Hemiplegic, a, 833 

gait, 834 
Hemicrania, 221 
Hemihypertrophy, 343 
Hemispasm, 772 
Hemianaesthesia, Jjy 
Hemorrhage, spinal meningeal, 524 

spinal, 528 

cerebral, 828 

ventricular, 836 
Hemorrhagic encephalitis, 865 

pachymeningitis, 794 
Hephaestic hemiplegia, 281 
Hereditary chorea, 297 

trophcedema, 321 

ataxic paraplegia, 443 

ataxia, 444 

cerebellar ataxia, 444 

bulbar paralysis, 953 
Heredity, 26 
Herpes, 970 
Heterotopia. 570 



Hysterogenic zones, 11 1 

Higher centers, 747 

Hoffmann's sign, 260 

Homonymous hemianopsia, 783, 789 

Horrors, 961 

Huntington's chorea, 297 

Hydatid, spinal, 509 

Hydromyelia, 563 j 

Hydrorrhachis externa, 569 

Hydrocephalus, 938 

acute, 814 
Hydrocephalic cry, 817 
Hydrocephaloid anaemia, 824 
Hydrops, articular, 321 
Hydrophobia, 968 
Hydrotherapy, 82 
Hydroencephalocele, 957 
Hyperaesthesia, 47 
Hypaesthesia, 47 
Hyperalgesia, 48 
Hyperosmia, 780 

Hyperthyroidation, 323 ' 

Hypertrophy, 74 
Hypertrophic pachymeningitis, 514 

osteo-arthropathy, 345 

neuritis of infants, 454 
Hyperaemia, spinal, 527 

cerebral, 825 
Hyperkinesis, 52 
Hyperidrosis, 74 
Hypoglossal tic, 266 
Hypochondriasis, 173 
Hypophysis cerebri, 739 
Hypnotism, 142, 143 
Hypnosis, 145 
Hysteria, 102 

Hysterical chorea, 132. 299 
Hystero-epilepsy, 120 
Hystericus, status, 122 

globus, 119 

I 
Ideas, 764 

Idiocy, amaurotic family, 451 
Idiopathic reflex irritability, 63 
Illusion, 756 
Incoordination, 53 
Indirect pyramidal tracts, 472 
Infection, 33 
Infantile hemiplegia, 854 

palsy, 541 

meningitis, chronic, 820 

convulsions, 252 
Influenza, 971 

Ingravescent apoplexy, 837 
Inherited diseases, 100 



980 



GENERAL INDEX 



Inhibition, 746 
Inhibiting lobe, 747 
Inhibitory functions, 721 
Inion, 679 
Inference. 184 
Infectious polyneuritis, 599 
Incisures, Lantermann's, 579 
Inflammation, 38 

interstitial, 579 

parenchymatous, 579 
Internal capsule, 736 
Intermittent incontinence of urine, 480 
Intercostal neuralgia, 251 
Interstitial hypertrophic neuritis, 454 
Interstitial nervous diseases, 457 

inflammation, 579 

neuritis, 581 
Intracranial aneurism, 934 

sinuses, 661 

veins, thrombosis of, 850 

sinuses, thrombosis of, 850 
Intoxication, 33 

vertigo, 155 

lead, 595 
Intermittent articular hydrops, 321 
Intentional tremor, 905 
Intellectual states, abnormal, 756 
Insomnia, 146 
Iodothyrin, 323 
Irritation, spinal, 505 

sensory, 779 
Irritability, 19 

Iridochoroiditis, purulent, 811 
Ischuria paradoxa, 480 
Ischiadic neuralgia, 627 



Jaw, reflex, 62 
clonus, 62 
Jacksonian epilepsy, 188, 206 



Kakke, 590, 603 

Karyochrome, 93 

Keratitis, neuroparalytic, 651 

Kernig's sign, 517, 803 

Knies' obstructive optic neuritis, 870 

Korsakoff's syndrome, 594 

Kubisagara, 156 

Kyphosis, 341, 501, 508 

L 
Latafi, 270 
Laryngeal crises, 382 
Lambda, 679 
Lancisi, nerves of, 687 
Labile current, 85 



Lateral curvature, 509 

limiting layer, 476 
Language, disturbances of, 763 
Laryngeal paralysis, 660 
Lantermann's incisures, 579 
Landry's paralysis, 431 
Lancinating pains, 375 
Layer, ambiguous, 683 
Lead palsy, 619 

intoxication, 595 
Lenticular nucleus, 690 
Lesser zone, 475 
Leprosy, anaesthetic, 568 
Leontiasis ossea, 343 
Lethargy, 146 
Leptomeningitis, intracranial, 798 

spinal, 516 
Leprous polyneuritis, 604, 611 
Lipoma of the brain, 910 
Lipomatous muscular atrophy, 416 
Little's disease, 421, 425, 854 
Ligamentum dentatum, 462 
Lissauer's zone, 476 
Lobar sclerosis, 857 
Lobes, cerebral, 672 
Lobe, inhibiting, 747 
Local asphyxia, 310 

thermometry, 74 
Lockjaw, 965 
Locomotor ataxia, 367 
Localization schools, 716 

cerebral,' 662, 714 

spinal, 459, 485 
Longitudinal fasciculus, posterior, 699 
Lordosis, 417 
Lower arm palsy, 616 
Loss of consciousness, 760 
Lumbo-sacral myelitis, 536 
Lumbar neuralgia, 251 

enlargement, 463 

puncture, 459, 493, 8c6 

plexus, 624 
Luy's body, 695 
Lyssophobia, 969 
Lyssa, 968 

M 

Macroaesthesia, 48 
Mortui, digiti, 311 
Macropodia, 343 
Macrocheiria, 343 
Magrums, 297 
Mai, petit, 188, 204 
grand, 188, 200 
Malignant meningitis, 81 t 
Malingering, 133, 186 



GENERAL INDEX 



98l 



Malum cotunnii, 627 
Malformations of the brain, 956 

of the cord, 569 
Malarial coma, 762 
Mania, Bell's, 874 
Main-en-griffe, 515, 623 
Marriage, 77 
Marrow, spinal, 461 
Marantic thrombosis, 850 
Mariotte, blind spot of, 781 
Mastodynia, 251 
Masochism, 170 
Masticatory tic, 266 
Masturbation, 169 
Massage, 84 
Matter, nervous, 17 

gray and white, 97 
Mater, dura, 461, 665 

pia, 462, 667 
Mechanico-therapy, 83 
Medulla oblongata, 740 

oblongata, diseases of, 948 

oblongata, tumor of, 923 

olfactorius. 687 

spinalis, 461 
Medullary substance, 91 
Medicinal treatment, 87 
Megalopsia, 792 
Megalocephalic brain, 664 
Magalocephaly, 343 
Megrims, 297 
Melancholia, 162, 174 
Membranes, spinal, diseases of, 511 

of brain, 665 

of the brain, diseases, 793 
Mental failure, 762 

paralysis, 776 
Meniere's disease, 153, 657 
Meningitis, granular, 815 

chronic, 820 

syphilitic spina 1 , 519 

gummatous, 521, 878 

pneumococcus, 813 

tuberculous, 814 

serous, 820, 939 

malignant, 81 1 

ossifying, chronic, 820 

epidemic cerebrospinal, 808 

chronic infantile, 820 

spinal, 512 

basilar, 814 
Meningeal hemorrhage, spinal, 524 
Meningo-myelitis. syphilitic, 523 
Meningomyelocele, 569 
Meningoencephalitis. 864 
Meningocele. 569, 957 



Meningomyelitis, 531 

Mesencephalon, 668 

Meriatschenje, 270 

Mercurial polyneuritis, 598 

Metasyphilis, 367 

Metencephalon, 668 

Metatarsalgia, Morton's, 633 

Micromegaly, 343 

Micropsia, 792 

Microcephalic brain. 664 

Microgyria, 857 

Micrencephaly, 957 

Micromyelia, 570 

Microcephaly, 957 

Middle fossa, tumor of, 926 

Migraine, 221 

Mitral cells, 688 

Miliary aneurisms, 828 

Minor chorea, 287 

Mind, the, 129, 140, 754 

Miryachit, 270 

Mode of life, 31 

Mogiphonia, 282 

Mogigraphia, 273 

Monroe, groove of, 669 

Monospasm, 724, 772 

Monocular diplopia, 792 

Monoplegia, 51, 773 

Morphinomania, 963 

Morphinism, 963 

Morphine habit, 963 

Morton's fluid, 570 

Morvan's disease, 568, 623 

Morbus sacer, 188 

Motor projection paths, 359, 483, 710 

segment, 361 

symptoms, 50 

areas, 723 

aphasia, 767, 768 
Movements, associated. 776 
Multiplex, paramyoclonus, 271 
Multiple sclerosis, 901 

neuritis, 589, 454 

neuromata. I 1 
Muscat volitantes, 166 
Muscles and their functions, 636 

rubber, 621 
Muscular sense, 721 

insanity, 20J 
Mutism, hysterical, 1J4 

Myasthenia gravis, l-'o 

Myelencephalon, WhX 
My el o- encephalitis, 864 

Myelitis. 531 

syphilitic, 522 

1 Myelinic neuroma, 609 



982 



GENERAL INDEX 



Myelocele, 569 
Myelomalacia, 500 
Myokymia, 167, 264 
Myoclonus-epilepsy, 207 
Myoclonia, 264, 271 
Myospasia, 271 
Myospasm, 262 
Myotatic irritability, 60 
Myositis of the diaphragm, 613 
Myospasia impulsiva, 269 
Myotonia congenita, 284 
Myosclerosis, 411 
Myxcedema, 335 
Myxoma of the brain, 910 



Narcosis, opium, 762 
Nausea, 752 

Nationality in etiology, 31 
Necrobiosis, 39, 846 
Nerves, spinal, diseases of, 613 
• dorsal, 624 

phrenic, 613 

posterior thoracic, 614, 617 

suprascapular, 614, 618 

rhomboid, 614 

subclavian, 614 

anterior thoracic, 614 

musculocutaneous, 614, 618 

median, 614, 621 

of Wrisberg, 614 

internal cutaneous, 614 

ulnar, 614, 622 

subscapular, 614 

circumflex, 614, 618 

musculo-spiral, 614, 619 

dorsal, 624 

obturator, 626 

anterior crural, 626 

external cutaneous, 626 

superior gluteal, 626 

external popliteal, 634 

internal popliteal, 635 

tibialis posticus, 635 

plantar, 635 

cranial, diseases of, 643 

olfactory, 643, 688 

optic, 643 

oculomotor, or third, 646 

trochlear, patheticus, fourth, 648 

abducens, or sixth, 648 

trifacial, trigeminal, fifth, 649 

pudic, 626 

sciatic, 626 

peroneal, 627, 634 

facial, or seventh, 652 



Nerves — 

artist's, 653 

auditory, or eighth, 657 

glossopharyngeal, or ninth, 658 

pneumogastric, tenth, 659 

accessorius, eleventh, 660 

hypoglossal, twelfth, 661 

of Wrisberg, 700 

energy, specific, 243 

diseases of, 576 

anatomy of, 576 

tumors of, 609 

the, 460, 577 

sympathetic, 306 
Nervous system, the, 17 

matter, 17 

organ, 20 

apparatus, 97 

dyspepsia, 168 
Nervi erigentes, 308 
Neuroses, 102 
Neuroses, traumatic, 182, 575 

fear, 163 

occupation, 272 
Neuralgia, 242 

sciatic, 633 
Neuro-retinitis, 784 
Neurone, the, 91 
Neurone doctrine, the, 89 
Neuronic diseases, 89 

functions and symptoms, 460 
Neural tube, 668 
Neuralgia ischiadica, 627 
Neuroma, plexiform, 610 

true and false, 609 
Neuromata, 609 

multiple, 609 
Neurotization, 585 
Neuritis, 581 

optic, 784, 787 

retrobulbar, 787 

Knies' obstructive, 870 

multiple syphilitic, 886 

sciatic, 633 

focal, 629 

multiple gummatous, 521 

hypertrophic, 454 

multiple, 454, 589 
Neuroglia, 95, 457 
Neuromyelitis, 454 
Neuroparalytic keratitis, 651 
Neurofibromatosis, 612 
Neuropathy, 28 
Neuropathic headache, 236 
Neuronic architecture, 96 
Neurotic vertigo, 155 



GENERAL INDEX 



98, 



Neurasthenia, 157 
Neuraxone, 91 
Neurilemma, 91 
Neighborhood symptoms, 718 
Negro lethargy, 148 
Nocturnus, pavor, 141 
Nigra, substantia, 695 
Non-neuronic diseases, 457 
Nocturnus, favor, 141 
Node of Ranvier, 578 
Nodal neuritis, disseminated, 584 
Nucleus, motoroculi, 699 

trigeminal, 699 

of Dieter, 703 

dentatus, 739 

emboliformis, 707 

fastigium, 707 

globosus, 707 

caudate, 690 

lenticular, 690 

red, 692, 695, 739 

tegmenti, 695. 739 

of Bechterew, 704 

accessorius, 704 

vago-glosso-pharyngeal, 704 

ambiguus, 705 

hypoglossal, 705 

facial, 700 
Nuclei, auditory, 703 

pontile, 741 

nodal, 705, 741 

cranial nerve, 698, 741 

gracilis and cuneatus, 475 
Nutans, spasmus, 268 
Nymphomania, 381 
Nystagmus, 449, 905 



Obstetrical palsy, 617 
Obsession, 163, 759 
Occipital neuralgia, 250 

lobes, tumor of, 921 
Occupation muscular atrophy, 430 

neuroses, 272 

in etiology, 31 
Ocular palsy, periodical, 647 

vertigo, 152 
(Edema, angioneurotic, 318 
Olfactory paresthesia, 780 

hallucinations,. 780 

area, 722 

lobes, 686 

glomerulus, 688 

symptoms, 779 
Olivary bodies, 7°5, 741 
Ophthalmoplegia, 427, 950 



Opisthotonos, 810 

cervical, of infants, 820 
Opium habit, 963 

narcosis, 762 
Optic thalami, 691, 737 

tracts, 692 

chiasm, 694, 788 

neuritis, 784, 787 

atrophy, 784, 787 

symptoms, 780 
Operculum, 675 
Oppenheim's reflex, 57 
Organ, the nervous, 20 
Organo-therapy, 88 
Organic headache, 237 

diseases, 101 
Orthotonos, 810 
Ossea, leontiasis, 343 
Ossifying meningitis, 820 
Osteoma of the brain, 910 
Osteomyelitis, 550 
Osteitis deformans, 343 
Osteo-arthropathy, hypertrophic, 345 



Pachydermatocele, 610 
Pachymeningitis, 793 

interna, 794 

externa, 512, 794 

cervical hypertrophic, 514 
Pacchionian bodies, 667 
Pachyakria, 339 
Paget's disease. 343 
Pain, 242 
Palpitation, 168 
Palmus, 269 
Palmar reflex, 56 
Pallidus, globus, 690 
Palsy, infantile, 541 

craft, 430, 621 

professional, 430. 621 

arthritic, 617 

obstetrical, 017 

serratus, 617 

had, 619 

cerebral, of childhood, 854 

l.rb's, 616 

upper arm, 616 

Klumpke's, 616 

lower arm. 6l6 

facial, 653 

Bell's, 653 

rheumatic, 653 

refrigeratory, 653 

crutch, 581, 620 

recurrent ocular, 047 



9 8 4 



GENERAL INDEX 



Pantophobia, 163 
Pantomimic aphasia, 767, 771 
Pantomime, 771 
Panophthalmitis, 651 
Papillitis, 784 
Paralysis, 51 

compression, 619 

analgesic, 623 

apoplectiform bulbar, 952 

diver's, 570 

atrophic spinal, 541 

craft, 581 

drunkards, 581 

acute ascending, 431 

Landry's, 431 

agitans, 299 

periodical, 436 

hereditary bulbar, 953 

crossed, 924 

compressed air, 570* 

crossed, 655 

psychic, 776 

pseudo-bulbar, 766, 774 

laryngeal, 660 

diaphragmatic, 613 
Paralytic chorea, 291 

vertigo, 156 
Paralytica, dementia, 888 
Parry's disease, 322 
Partial epilepsy, 188, 206 
Paroxysmal headache, 226 
Parkinson's disease, 299 
Paresis, 51 

general, 888 
Parietal lobes, tumor of, 919 
Parenchymatous neuritis, 581 
Paraldehyde habit, 96 
Parasyphilis, 367 
Parturient convulsions, 254 
Paramyoclonus multiplex, 271 
Paraplegia, 51 

dolorosa, 508 

syphilitic, 522 

cerebral, 854 

spastic, 421 

ataxic, 439 
Paradoxical ischuria, 480 

muscular contraction, 64 
Paraphasia, 767 
Paresthesia, 47 
Paramimia, 771 

Parenchymatous inflammation, 579 
Paraplasm, 93 
Paresthesia?, 971 

Pars intermedia of Wrisberg, 652 
Patella reflex, 58 



Pathology, general, 35 
Patient, examination of, 41 
Path, corticopetal, 733 

corticofugal, 733 
Paths, afferent and efferent, 98 
Pavor nocturnus, 141, 757 
Pederasty, 170 
Peripheral nerves, diseases of, 576 

nerves, anatomy of, 576 
Perforating ulcer, 383 
Perineuritis, 581 
Pertussis, 971 
Periodical paralysis, 436 

ocular palsy, 647 
Perversion, sexual, 170 
Peripheral nerves, pathology of, 579 
Peroneal atrophy, 399 
Perimeter, 780 
Periependymal myelitis, 537 
Perikaryon, 93 
Perineurium, 577 
Pes equino-varus, 548 

calcaneus, 548 

anserinus, 653 

pedunculi, 697 
Petit mal, 188, 204 
Pharyngeal crises, 382 
Phobia, 107, 163, 759 
Phlebitis, 851 
Phrenic nerve, 613 
Physiology of the brain, 714 
Physiological cup, 784 

scotoma, 781 
Physical exercise, 79 
Pia mater, 462, 667 
Pineal gland, 695, 739 
Pianist's cramp, 273 
Pied-en-griffe, 634 
Pituitary body, 739 
Plexus, brachial, 614 

palsy, brachial, 616 

lumbar, 624 

sacral, 626 

coccygeal, 626 
Plexiform neuroma, 610 
Plantar neuralgia, 252 
Pleurothotonos, 966 
Pneumonia, aspiration, 660 
Pneumococcus meningitis, 813 
Pododynia, 252 
Polyneuritis, 589 

senile, 590 

alcoholic, 592 

toxic, 592 

lead, 595 

saturnine, 595 



GENERAL INDEX 



985 



Polyneuritis — 

arsenical, 597 

argentic, 598 

mercurial, 598 

syphilitic, 598 

infectious, 599 

diphtheritic, 599 

rheumatic, 602 

puerperal, 602 

diabetic, 603 

endemic, 603 

leprous, 604, 611 
Poliomyelitis, 532 

anterior acute, 541 

of adults, 552 
Poliomyelitis, 532 
Polioencephalitis, 409, 855, 864 

acute inferior, 951 

acute superior, 951 
Polyclonia, 271 
Polyaesthesia, 48 
Pons Varolii, 740 

tumor of, 923 

diseases of, 948 
Pontile abscess, 871 
Porencephaly, 856, 957 
Postero-median tracts, 475, 484 
Postero-lateral tracts, 475, 484 
Postero-internal radicular zone, 475 
Posterior longitudinal fasciculus, 699 

fossa, tumor of, 926 

spinal sclerosis, 367 
Post-hemiplegic chorea, 297 
Pott's disease, 499 
Potamophobia, 163 
Precuneus, 676 
Pre-hemiplegic chorea, 297 
Pressure aphasia, 771 
Preacher's hand, 515 
Progressive stupor, 883 

hypertrophic neuritis, 454 

muscular atrophy, 392 

bulbar paralysis, 395, 406, 951 

muscular dystrophy, 409 

hemiplegia, 885 
Progression, cross-legged, 424, 858 
Protopathic atrophy, 393 
Proto-albumose, 495 
Prosencephalon, 668 
Procursive chorea, 299 
Projection path, motor, 359, 483, 710 

tracts, 472, 710 
Professional palsy, 430 
Protoplasm, 93 
Protoplasmic process, 91 
Primary diseases, 20 



Pruritis, 971 
Prophylaxis, 77 
Prosopalgia, 248 
Prosopoplegia, 653 
Prostatorrhcea, 170 
Primary degeneration, 61 
Pseudoclonus, 61 

tetanus, 256 

tabes, 384, 597, 605 

ptosis, 124 

hypertrophy, 74 

hypertrophic paralysis, 416 

atrophy, 74 

hydrophobia, 969 

bulbar paralysis, 766, 774, 952 

meningitis, 806 

paralysis, 51 

reminiscence, 595 
Psychosis, 717, 754 
Psychic headache, 237 

epileps)^, 188 

blindness, 791 

paralysis, 776 

symptoms, 45, 753 
Psychoneuroses, 102 
Psychomotor centers, 729 
Psychology, voluntaristic, 754 
Psyclampsia, 759 
Psychalgia, 162, 760 
Psammoma of the brain, 910 
Ptosis, 647 
Pterion, 679 

Puncture, lumbar, 459, 493, 806 
Pupillary reflex, 63, 780 
Pulvinar, 691, 738 
Puncta dolorosa, 629 
Purkinje, cells of, 707 
Putamen, 690 
Pulse, 752 

Purulent inflammation, 39 
Pyramidal tracts, 472 
Pyrosis, 168 
Pyrocatechin, 495 



Quadriplegia, 536, 604 
Quadrigemina, corpora, 692, 695, 738 



Rabies, 968 
Rachischisis, 569 
Rachitis, 550 
Radiations of Gratioli 

Radicular zones, 475 



986 



GENERAL INDEX 



Rami efferentes, 308 

communicantes, 308 
Ranvier, node of, 578 
Raynaud's disease, 310 
Reaction of degeneration, 70 

a distance, 585 

of excitation, 260 
Rectal crises, 382 
Rectus clonus, 442 
Receptive centers, 717 
Red nucleus, 692, 695 
Reflex action, spinal, 476, 477 

headache, 236 

epilepsy, 191 

causes of disease, 34 

action, automatic, 476 

action, 55 
Refrigeratory palsy, 653 
Reinforcement, 59 
Regeneration, 39, 585 
Regio subthalamica, 695 
Renal crises, 382 

symptoms, 753 
Respiration, 753 
Respiratory tic, 266 

crises, 382 
Rest-cure, 178 
Retina, 692 

Retrobulbar neuritis, 787 
Rheumatic palsy, 653 

polyneuritis, 602 
Rhinencephalon, 686 
Ring scotoma, 117 
Rinne's test, 
Risus sardonicus, 066 
Root-zone, anterior fundamental, 476 
Rodagen, 331 
Rubber muscles, 621 



Sacral plexus, 626 
Sadism, 170 
Salivation, 74 
Saltatoric spasm, 120 
Sand, brain, 696 
Sardonic grin, 966 
Sarcoma of the brain, 910 
Saturnine encephalopathy, 596 
Satyriasis, 381 
Scanning speech, 767 
Scapulo-humeral reflex, 62 
humeral dystrophy, 418 
Scaphoid abdomen, 803 
Schools, localization, 716 
Sciatica, 251, 627 



Sclerosis, disseminated, 901 

lobar, 857 

multiple, 901 

amyotrophic lateral, 395, 401 
Sclerosis, 39 

posterior spinal, 367 
Sclerodactyly, 347 
Scleroderma, 346 
Scoliosis, 631 
Scotoma, 781, 782 

physiological, 781 

central, 787 

ring, 117 
Scrivener's palsy, 273 
Secondary diseases, 21, 458 

spastic paralyses, 426 

degenerations, 458, 580 
Secretory symptoms, 74 

reflexes, 63 
Segment, motor, 361 
Self-nutrition, 19 
Semicircular canals, 149 
Seminal emission, 170 
Sense, muscular, 721 

stereognostic, 721 

sphere, 728 
Sensitive-motor zone, 739 
Senile epilepsy, 191 
Sensory symptoms, 46 

aphasia, 769 

irritation, 779 

projection path, 363, 710 
Sensorial areas, 719 
Serum-therapy, 88 
Serous meningitis, 820, 939 
Serratus palsy, 617 
Sex in etiology, 31 
Sexual perversion, 170 
Shoemaker's spasm, 256 
Shaking palsy, 299 
Sinuses, intracranial, 666 
Simulation, 186 
Sinus thrombosis, 850 
Skin reflexes, 56 
Skiagraphy, 75, 561, 929 
Sleep, 141 

Sleeping sickness, 148 
Solitary fasciculus, 704 
Softening, 39 
Spasmus nutans, 268 
Spasmodic torticollis, 267 
Spastic paralysis, 51 
Spasm, 52, 262, 772 
Spasmodic tic, 264 

paraplegia, 421 
Space, subarachnoid, 462 



GEXERAL INDEX 



987 



Speech, 45, 763 

scanning, 767 

staccato, 767 

voluntary, 769 

disturbances of, 763 
Specific nerve-energy, 243 
Spermatic neuralgia, 252 
Spermatorrhoea, 170 
Spinal hydatid disease, 509 

arthritis deformans, 510 

membranes, diseases of, 511 

meningitis, 512 

leptomeningitis, 516 

paralysis, Erb's, 523 

meningeal hemorrhage, 524 

cord diseases. 526 

anaemia, 527 

hypersemia, 527 

asymmetry, 570 

concussion, 574 

centers, 480 

column, diseases of, 496 

marrow, 461 

cord cavities, 562 

embolism, 528 

thrombosis, 528 

endarteritis, 528 

hemorrhage, 528 

apoplexy, 529 

paralysis, atrophic, 541 

cord abscess, 555 

cord tumor, 555 

cord, anatomy, etc., 459 

localization, 459, 485 

topography, 459, 485 

nerves, diseases of, 613 

irritation, 505 

syphilis, 519 
Spina bifida, 569 
Spotted fever, 808 
Spondylitis, tubercular, 499 
Spontaneous movements, 379 
St. Vitus' dance, 287 
Static ataxia, 377 
Status hystericus, 122 

epilepticus, 189, 207 

hemicranicus, 230 
Staccato speech, 767 
Stabile current, 85 
Stammering, 282 
Stephanion, 679 
Stellwag's symptom, 328 
Striae of Bechterew, 683 

acusticae, 704 
Striate bodies, 689, 737 
Struma, 324 



Stupor progressive, 883 
Stuttering, 266, 282 

hysterical, 124 
Substantia gelatinosa, 469 

nigra, 695 
Subthalamic region, 695 
Suggestion, 143 
Sulci, cerebral, 672 

arterise, 465 
Suspension treatment, 390 
Sydenham's disease, 287 
Sympathetic nerves, 306 

disease symptoms, 309 
Symptoms, psychic, 45 

motor, 50 

sensory, 46 

vasomotor, 72 

secretory, 74 

trophic, 74 

neighborhood, 718 

of spinal cord disease, 459 
Symptomatology, general, 41 
Symptomatic epilepsy, 206 
Symbol, 764 

Symmetrical gangrene, 310 
Synapse, 91 
Somatochrome, 93 
Syphilis, cerebral, 877 

spinal, 519 
Syphilitic myelitis, 522 

paraplegia, 522 

meningo-myelitis, S23 

polyneuritis, 598 

disease of vertebrae, 509 

spinal meningitis, 519 

pseudo-tabes, 384 
Syphiloma of the cord, 522 

of the brain, 910 
Suppurative encephalitis, 867 
System diseases, 350, 356 

the nervous, 17 
Syringomyelocele, 569 
Syringomyelia, 563 
Swelling, giant, 318 



Tabes dorsalis, 367 

Tache cerebralr. 804 
bleuatre, ^\j. 74 

Tactile aphasia, 771 
Tachycardia. 324 
Talipes calcaneus, 635 

valgus, 548 
Tangential fibres, 683 
Tegmentum. 697 



988 



GENERAL INDEX 



Telodendrion, 91 
Telegrapher's cramp, 273 
Telencephalon, 668 
Temperature crises, 382 
Temporal lobes, tumor of, 921 
Temperature, 752 
Tendon reflexes, 57 
Tetany, 256 
Tetanilla, 256 
Tetanus, 965 

pseudo, 256 
Thermo-anaesthesia, 2>77 
Thermometry, local, 74 

general, 75 
Therapy, symptomatic, 81 
Thermanaesthesia, 48 
Thrombosis, cerebral, 845 

of the sinuses, 850 

spinal, 528 
Thalamencephalon, 668 
Thalami, optic, 691, 737 
Thomsen's disease, 284 
Thyroiodin, 323 
Tic impulsif, 269 

de pensee, 270 

spasmodic, 264 

convulsif, 264 

facial, 265 

douloureux, 248 
Tinnitus aurium, 166 
Titubation, 055 
Tobacco heart, 169 
Tonic spasm, 52 

influence, spinal, 476, 481 
Topoalgia, 48 
Topography, spinal, 459, 485 

cranio-cerebral, 677 
Torticollis, spasmodic, 267 
Toxic headache, 236 

polyneuritis, 592 
Traumata, 33 
Traumatic neuroses, 182, 575 

epilepsy, 190 
Tracts, optic, 692 
Tractus tegmento-cerebellaris, 695 

cortico-spinalis, 698 
Tremor, 53 

intentional, 905 
Tremens, delirium, 960 
Treatment, general, 75 
Triceps reflex, 62 
Trigeminal neuralgia, 248 
•Trismus, 966 
Trophic symptoms, 74 

influence, spinal, 476, 481 
T*ophoedema, hereditary, 320 



Trousseau's sign, 260 
Trophoneuroses, 74, 306 
Tube, neural, 668 
Tubercular spondylitis, 499 
Tubercula dolorosa, 611 
Tuberculous meningitis, 814 
Tuberosa, urticaria, 318 
Tubercle of the brain, 910 
Tubular vision, 112 
Tumor of the spinal cord, 555 
of the cauda, 557, 559 
of the brain, 909 
of the vertebrae, 507 
Tumors of the nerves, 509 
Turck's column, 472 
Tussis hysterica, 119 
Tympani, chorda, 701 



Uraemic convulsions, 255 

coma, 761 
Uncrossed pyramidal tracts, 472, 483; 
Upper arm palsy, 616 
Urticaria, 970 

tuberosa, 318 

giant, 320 

factitia, 168 
Urethrodynia, 252 

V 

Vacuolation, 36 
Valleix's points, 586, 629 
Vasomotor symptoms, 72 

reflexes, 63 

action, 476 
Vasocorona, 465 
Veins of the brain, 714 
Venae Galeni, 714 
Ventricular hemorrhage, 836 

zone, 475 
Ventral cerebro-spinal fasciculus, 476* 
Vertebrate animal, 459 
Vertebrae, diseases of, 496 

caries of, 499 

tumors of, 507 

syphilis of, 509 

erosion of, 509 
Vertigo, 55, 149, 752 

ocular, 152 

aural, 153 
Vermis, 705 
Vesicular columns, 469 
Vesicles of the brain, 668 
Vicq d'Azyr, line of, 682 
Visceral reflexes, 63 

neuralgia, 252 



GENERAL INDEX 



989 



Vision, tubular, 112 
Visual disturbances, 780 

aphasia, 770 

field, contraction of, 780 

area, 722 
Vitse, arbor, 707 
Vita sexualis, 191 
Volitantes, muscae, 166 
Voluntary speech, 169 
Voluntaristic psychology. 754 
Vomiting, 751 
Von Graefe's sign, 327 

W 

Wallerian degeneration, 37. 351, 584 

Weber's test, 792 

Weight of brain, 664 

"Weir Mitchell treatment, 178 



Weigert-Edinger hypothesis, 
Wet brain, 806 
White matter, 97 
Willis, circle of, 711 
Word-deafness, 723, 762, 769 

blindness, 762, 770 
Wrist reflex, 62 

drop, 566, 619 
Wrisberg, nerve of, 700 
Wryneck, spasmodic, 267 
Writer's cramp, 275 



Zone, hysterogenic, in 
sensitive-motor, 729 
Zones, radicular, 475 
Zona molecularis, 707 
granulosa, 707 



357 



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